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Results for “Cell Proliferation”

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PubMed1991

The MTT-assay as a rapid test for cell proliferation and cell killing: application to human peripheral blood lymphocytes (PBL).

The possibility to use the colorimetric MTT assay for measuring proliferation and cell death of human peripheral blood lymphocytes (PBL) was studied. In a range from 100,000-800,000 cells/well a linear correlation between the optical signal (OD signal at 570 nm) and the cell number was found. It is necessary to incubate the cells with the MTT at least 2 hours. After stimulation by different PHA concentrations a very good correlation between [3H] thymidine incorporation and MTT assay was found. A comparison of daunomycin cytotoxicity, measurement by trypan blue exclusion and MTT assay, gave also a good correlation between both methods. It can be pronounced that the MTT assay is a suitable method to measure cell proliferation and cell death of human PBL. The assay is easy to handle, a large number of probes can be assayed in a relatively short time and no radioactivity is necessary. For the measurement of the colored product a common ELISA reader can be used.

Cell Death↗

PubMed1984

Influence of cell proliferation and cell cycle phase on expression of estrogen receptor in MCF-7 breast cancer cells.

In the present study, the effects of cell cycle phase and proliferation rate on the expression of specific estrogen binding activity were explored in hormone-dependent human breast cancer cells. A technique was developed to alter the proliferative rate of MCF-7 cells by plating at different densities. The doubling time ranged from 20 to 48 hr, showing a negative relation to the number of plated cells. Slowly proliferating cells had accumulated more than twice as much estrogen receptor (ER) activity as did fast-proliferating cells. Exposure of exponentially growing cells to isoleucine-deficient medium resulted in decreased thymidine incorporation and disappearance of detectable cellular ER activity. Overall protein synthesis was reduced by only 30% in cells growing in isoleucine-free medium. At 24 hr after release from isoleucine deprivation, ER levels are fully restored, although thymidine incorporation does not resume for an additional 6 to 8 hr, and increases in cell number are not seen for 24 hr. Exposure of exponentially growing cells to 2 mM thymidine for 24 hr produced partially synchronized MCF-7 cells (approximately 70%). Six hr after release from excess thymidine, cells reached S phase; after 9 hr, G2; and after 18 hr, G1. ER levels immediately and, 6 hr after release, remained unchanged, showed a slight increase at 9 hr, and showed an increase of about 50 to 60% at 18 hr. These data suggest that: (a) ER binding activity and DNA synthesis can be dissociated; (b) ongoing protein synthesis is necessary for maintenance of cellular ER activity; and (c) ER is apparently synthesized throughout the cell cycle, with some evidence that this is predominantly in G1 and G2.

Breast Neoplasms↗

PubMed1993

Studies of the relationship between cell proliferation and cell death. III. AP-1 DNA-binding activity during concanavalin A-induced proliferation or dexamethasone-induced apoptosis of rat thymocytes.

In previous papers we started to investigate the possible relationship existing between cell proliferation and cell death. We reported that in rat thymocytes, undergoing cell proliferation upon stimulation with Concanavalin A or cell death following dexamethasone treatment, an induction of c-fos and c-jun occurs with different but partially overlapping kinetics (Grassilli et al., BBRC, 1992, 188, 1261-1266). To test the hypothesis that, in both processes, the early induction of these nuclear oncogenes is necessary to allow the induction of later-expressed genes regulated at the transcriptional level by AP-1 complex, AP-1 DNA-binding activity was investigated in the aforementioned model. Indeed, we found that AP-1 is activated not only in proliferating but also in apoptotic cells, with a kinetics in accord with our data about c-fos and c-jun mRNA accumulation in the same experimental model. Moreover, our findings suggest that an interaction between AP-1 and glucocorticoid receptor also occurs in our model of dexamethasone-mediated apoptosis.

Animals↗

PubMed2000

Involvement of cyclins in cell proliferation and their clinical implications in soft tissue smooth muscle tumors.

Expression of cyclins A and E and cyclin-dependent kinase 2 (cdk2) was examined immunohistochemically in 55 cases of soft tissue smooth muscle tumors, including vascular leiomyoma, and compared to expression of Ki-67 and proliferating cell nuclear antigen. Cyclin A was expressed in 70% of the leiomyoma cases, but with much lower labeling indexes than in leiomyosarcoma. Cyclin E was expressed exclusively in leiomyosarcoma. Although the differences of cyclin A- and cyclin E-labeling indexes between leiomyoma and leiomyosarcoma were statistically significant, no significant differences were found in the other markers. Furthermore, cyclin A- and/or E-positivity predicted a poor prognosis in recurrence- or metastasis-free survivals and overall survival. Immunoblotting revealed that cyclins A and E were expressed, in complex with cdk2, exclusively in tumors. In addition, not only leiomyosarcoma, but also leiomyoma specimens that exhibited negligible levels of complex expression, manifested detectable cdk2 activity. These results suggest 1) up-regulation of active cyclin A/cdk2 expression and associated kinase activity is critical for unrestrained cell proliferation; 2) cyclin E/cdk2 complexes may play a crucial role in leiomyosarcoma; 3) immunohistochemical detection of cyclins can be a more reliable tool for differential diagnosis between leiomyoma versus leiomyosarcoma than that of Ki-67 or proliferating cell nuclear antigen, and be a possible prognostic indicator.

Adult↗

PubMed2006

Proliferating cell nuclear antigen, survivin, and CD34 expressions in pancreatic cancer and their correlation with hypoxia-inducible factor 1alpha.

OBJECTIVE: Hypoxia-inducible factor 1alpha (HIF-1alpha) has been universally detected in many types of cells and plays a key role in modulation of tumor-related genes. The purpose of this study was to explore the relationship between HIF-1alpha messenger RNA (mRNA) expression and biologic characteristics in pancreatic cancer, such as tumor angiogenesis, tumor cell proliferation, differentiation, apoptosis, and metastasis. METHODS: Reverse transcriptase-polymerase chain reaction was used to detect HIF-1alpha mRNA expression. The expressions of survivin, proliferating cell nuclear antigen (PCNA), and CD34 proteins were measured immunohistochemically. The correlation between the expression levels of HIF-1alpha mRNA and survivin, PCNA, and CD34 were analyzed. RESULTS: There was very significant difference in the expression of HIF-1alpha between the pancreatic cancer tissue and adjacent normal tissue (P < 0.01), but no significant difference was found among tumor histopathologic grades (P > 0.05). There was significant difference in the expression of HIF-1alpha mRNA between Japanese Pancreatic Society stages I to II and stages III to IV (P < 0.05). The expression of HIF-1alpha mRNA was closely correlated with the expression of survivin, PCNA, and CD34 proteins. CONCLUSION: The expression level of HIF-1alpha mRNA is surmised to have a significant correlation with tumor angiogenesis, cell proliferation, apoptosis, and metastasis. Inhibition of HIF-1alpha may be an important and approachable therapeutic target for pancreatic cancer.

Antigens, CD34↗

PubMed1991

Differential activity of recombinant lymphokines on mouse B cell proliferation and cell cycle progression are revealed by 5-bromo-2'-deoxyuridine/Hoechst 33258 dye flow cytometry.

Activation of resting mouse B cells with anti-mu chain antibodies (anti-mu) leads to cell proliferation. We have investigated the effect of recombinant T cell interleukins (IL 2 to IL 6) on such anti-mu-induced proliferation. No proliferative response was detected when IL 2, IL 3 and IL 6, either alone or in combination with anti-mu, were studied. Furthermore, neither IL 4 nor IL 5 could induce proliferation when added alone to B cell cultures. However, when combined with anti-mu, IL 4 as well as IL 5 stimulated cell growth. Analysis by 5-bromo-2'-deoxyuridine/Hoechst 33258 flow cytometry revealed distinct effects of IL 4 and IL 5 on B cell growth. In the presence of anti-mu, both IL 4 and IL 5 co-stimulated unfractionated splenic B cells. However, when B cells were separated into subpopulations by density, IL 4 proved to be a cell cycle progression factor, stimulating the majority of resting B cells to enter the cell cycle. In contrast, IL 5 had little effect on the resting fraction of B cells. Rather, IL 5 acted as a co-competence factor, stimulating predominantly low-density B cells. Following exposure of anti-mu alone, most B cells accumulated in the G1 of the second cycle. Upon addition of IL 4, the cells acquired the ability to progress into the next S phase compartment. Contrary to what is seen when B cells are stimulated by other mitogens, very few cells are in the G2 compartments after anti-mu plus IL 4 stimulation. This phenomenon was not due to a differential cell cycle progression rate. Our findings provide an analytical basis for fractionating cell-cycle-compartment-specific B cells for their molecular study.

Animals↗

PubMed2000

Proliferating cell nuclear antigen expression in mucoepidermoid carcinoma of salivary glands.

CONTEXT: Among the cytological and morphological properties of mucoepidermoid carcinoma, one of the most important criteria for measuring its biological behavior and aggressiveness is cell proliferation. In this way, immunohistochemical markers of cell proliferation have been found to be useful in tumor classification and have formed part of the prognostic and therapeutic studies of these pathologies. OBJECTIVE: To analyze 11 cases of mucoepidermoid carcinoma (MEC) using the proliferation activity marker (PCNA) and to determine its relationship to the grade of malignancy of these tumors. DESIGN: Correlation study. SETTING: Head and Neck Surgery Service of Heliópolis Hospital, São Paulo, Brazil. SAMPLE: Slides of 11 cases of primary mucoepidermoid carcinomas of salivary glands were prepared according to routine techniques employed in the Oral Pathology Department of the Dentistry Faculty of São Paulo University, Brazil. They were fixed in a 10% formaldehyde solution and stained with hematoxylin and eosin. After this preparation the tumors were classified as low, intermediate and high grade of malignancy, according to the criteria established by Seifert & Sobin and Auclair, Goode & Ellis. The slides were sent for immunohistochemical processing to evaluate the positivity of proliferating cell nuclear antigen using the streptavidin biotin technique. MAIN MEASUREMENT: The correlation between proliferating cell nuclear antigen expression and the histological malignancy grade in mucoepidermoid carcinoma of salivary glands. RESULTS: there were 4 cases (36%) of low grade, 4 cases (36%) of intermediate grade and 3 cases (27%) of high grade of malignancy. After a comparative study between histological features and immunohistochemical analysis, significant differences were observed (P < 0.01) for low, intermediate and high grades: 16.04%, 26.98% and 56.98% of proliferating cell nuclear antigen expression in mucoepidermoid carcinoma, respectively. CONCLUSION: The proliferating cell nuclear antigen expression increases with the grade of malignancy in mucoepidermoid carcinoma of salivary glands.

Adult↗

PubMed1992

The effect of sulfasalazine on bovine endothelial cell proliferation and cell cycle phase distribution. Comparison with olsalazine, 5-aminosalicylic acid, and sulfapyridine.

Sulfasalazine is used in the treatment of chronic inflammatory states, for example, in inflammatory bowel disease and to a lesser degree in rheumatoid arthritis. In chronic inflammation, the formation of new blood vessels may play a key role in maintaining the inflammatory state. This process is dependent on the activation and proliferation of the endothelial cells. To investigate the possible role of sulfasalazine and its metabolites, sulfapyridine and 5-aminosalicylic acid, we examined the effect of these drugs on vascular endothelial cell proliferation in vitro. Cultures of bovine aortic endothelial cells were incubated with sulfasalazine and its metabolites. At 24 hours of incubation, sulfasalazine inhibited tritiated thymidine incorporation and cell proliferation and had already slowed S-phase progression at a concentration greater than 0.125 mmol/L. After 3 hours of incubation, sulfasalazine inhibition of tritiated thymidine incorporation into the DNA of endothelial cells was observed. This inhibition was completely reversible 24 hours after the drug was removed. One of the possible mechanisms for the inhibition of endothelial cell proliferation is interference with the de novo synthesis of thymidine that depends on folate-dependent enzymes. The effect of deoxyuridine and tetrahydrofolate on tritiated thymidine incorporation into cellular DNA, as well as release of tritium to water by [5-3H]-labeled deoxyuridine on methylation to thymidine, were used as probes for the de novo synthesis of thymidine. Deoxyuridine and tetrahydrofolate, when added to cells either individually or together for 3 hours, suppressed incorporation of tritiated thymidine into DNA through an increase in de novo thymidine synthesis. Sulfasalazine, but not its metabolites, reduced this suppression.2+ culture is inhibited by sulfasalazine and olsalazine but not by their metabolites. This inhibition appears to depend partly on the reduction of de novo synthesis of thymidine that is folate dependent.

Aminosalicylic Acids↗

PubMed1992

Proliferating cell nuclear antigen counts in formalin-fixed paraffin-embedded tissue correlate with Ki-67 in fresh tissue.

Cell proliferation can be studied by a variety of techniques. However, most require fresh tissue. To evaluate cell proliferation in formalin-fixed paraffin-embedded sections, the authors immunohistochemically studied 35 tumors and 11 samples of normal/hyperplastic tissue with PC10, a monoclonal antibody directed against proliferating cell nuclear antigen. Results were compared with those obtained with Ki-67 on fresh tissues. There was no significant difference between proliferating cell nuclear antigen and Ki-67 counts, which were strongly correlated (r = 0.8). Proliferating cell nuclear antigen positivity was easier to evaluate because morphology was better preserved in formalin-fixed tissue. The authors conclude that PC10 is an alternative to Ki-67 in evaluating cell proliferation and has the advantage of reacting with formalin-fixed paraffin-embedded tissue.

Antibodies, Monoclonal↗

PubMed2002

The effects of a protease inhibitor fraction from tepary bean (Phaseolus acutifolius) on in vitro cell proliferation and cell adhesion of transformed cells.

Some protease inhibitors (PI), such as the soybean Bowman-Birk protease inhibitor (SBBI), have been described as anticarcinogenic agents. Although PI are ubiquitous compounds in living organisms, the anticarcinogenic potential of PIs other than SBBI remain poorly explored. We evaluated the antiproliferative effect of a protein fraction from tepary bean (Phaseolus acutifolius) seeds with protease inhibitor activity (TPIF), on normal and on malignant cells. TPIF was obtained after precipitation with ammonium sulfate and gel filtration, and its bioactivity was assayed in vitro on HeLa cells, normal 3T3 fibroblasts and 3T3/v-mos transformed fibroblasts. TPIF showed antiproliferative and cytotoxic effects on 3T3/v-mos transformed fibroblasts in a dose-dependent way. On the contrary, TPIF was only cytostatic for normal 3T3 cells at the highest doses assayed, and had no effect on epithelial HeLa cells proliferation. Sublethal TPIF doses also stimulated cell adhesion of poorly adherent 3T3/v-mos cell line.

3T3 Cells↗

PubMed1994

Comparison of villous trophoblast proliferation rate in hydatidiform mole and non-molar abortion by assessment of proliferating cell nuclear antigen expression.

This study examines the proliferative activity of trophoblast in hydatidiform mole, non-molar hydropic abortion and non-molar spontaneous abortion. Nine cases of complete mole, 10 cases of partial mole, eight cases of non-molar hydropic abortion and six cases of non-hydropic second trimester abortion were examined by routine histopathology and the rate of cell proliferation was assessed by immunoreactivity for proliferating cell nuclear antigen (PCNA). Hydropic abortion showed a significantly lower PCNA index than complete mole and partial mole. There was no significant difference in PCNA index between partial mole and non-hydropic abortion. The trophoblast of partial hydatidiform mole demonstrates significant cell proliferation but this, although higher than that of hydropic abortion, is no higher than that of non-hydropic abortion of a similar gestational age. The role of partial mole as a precursor of persistent gestational trophoblastis disease remains unclear.

Abortion, Spontaneous↗

PubMed1994

[Effects of plant polysaccharides on cell proliferation and cell membrane contents of sialic acid, phospholipid and cholesterol in S 180 and K 562 cells].

The four kinds of plant polysaccharides, i.e., pachyman polysaccharides (PPS), Acanthopanax senticosus polysaccharides (ASPS), polysaccharides of tremella fuciformis (TF) and lentinan, have obviously inhibitory action against the animal tumor growth and have been applied to the treatment of cancer. The mechanism was that they could enhance the body immune function, but whether the tumor cells were killed is not clear. In this paper, the effects of the four plant polysaccharides on cell proliferation in mice sarcoma (ascitic type) S180 and human chronic myelogenous leukemia K562 cells were studied with MTT chromometry. Tt was found That TF and lentinan had no effect on both cell line, but PPS and ASPS could obviously inhibit the proliferation of them, the IC50 of PPS was 1.5mg/ml in both cell line, that of ASPS was 0.38 mg/ml (S180 cells) and 0.28mg/ml (K562 cells) respectively. This result indicated that the PPS and ASPS were able to kill the tumor cell directly. To investigate the mechanism of antitumor action of PPS and ASPS, the sialic acid (SA), phospholipid (PI) and cholesterol (Ch) contents of S180 cell membrane were examined after the PPS or ASPS application for 24 hours. No significant changes were observed for the Ch and Ch/Pl ratio, the amount of SA increased and that of PI lowered respectively (P < 0.05). The results suggested that the antitumor action of PPS and ASPS not only related to the action of enhancing the body immune function but also related to the changes of cell membrane.

Animals↗

PubMed1997

Glomerular proliferating cell kinetics in acute post-streptococcal glomerulonephritis (APSGN).

To investigate the time sequence of glomerular cell proliferation in acute human glomerulonephritis, renal biopsy tissues were examined from 15 acute post-streptococcal glomerulonephritis (APSGN) patients (who were biopsied 1-31 days after onset), using an immunoperoxidase technique with monoclonal antibodies against proliferating cell nuclear antigen (PCNA) and various cell surface markers. Few, if any, PCNA+ cells were observed in normal glomeruli, but many cells were positive for PCNA in the acute phase of APSGN. Glomerular PCNA+ cells were observed either within glomerular tufts, or lining Bowman's capsule (parietal epithelial cells); the number of positive cells tended to decrease exponentially as the disease duration increased (r = -0.91, P < 0.0001). PCNA+ cells within glomerular tufts were further identified by double immunostaining. PCNA was not found in PMN or T cells, but a small proportion of macrophages were PCNA+. Most of the remaining PCNA+ cells were resident glomerular cells; the proportion of PCNA+ endothelial cells (CD31+) was over 80 per cent in the early phase, but as the disease continued the proportion of mesangial cells (alpha-smooth muscle actin+) increased to about half of the total PCNA+ cells within the tuft. These data indicate that the hypercellular glomeruli in APSGN are due not only to immune cell infiltration, but also to resident glomerular cell proliferation, probably induced by locally produced growth factors.

Acute Disease↗

PubMed1994

Integrated control of cell proliferation and cell death by the c-myc oncogene.

Regulation of multicellular architecture involves a dynamic equilibrium between cell proliferation, differentiation with consequent growth arrest, and cell death. Apoptosis is one particular form of active cell death that is extremely rapid and characterized by auto-destruction of chromatin, cellular blebbing and condensation, and vesicularization of internal components. The c-myc proto-oncogene encodes an essential component of the cell's proliferative machinery and its deregulated expression is implicated in most neoplasms. Intriguingly, c-myc can also act as a potent inducer of apoptosis. Myc-induced apoptosis occurs only in cells deprived of growth factors or forcibly arrested with cytostatic drugs. Myc-induced apoptosis is dependent upon the level at which it is expressed and deletion mapping shows that regions of c-Myc required for apoptosis overlap with regions necessary for co-transformation, autoregulation, inhibition of differentiation, transcriptional activation and sequence-specific DNA binding. Moreover, induction of apoptosis by c-Myc requires association with c-Myc's heterologous partner, Max. All of this strongly implies that c-Myc drives apoptosis through a transcriptional mechanism: presumably by modulation of target genes. Two simple models can be invoked to explain the induction of apoptosis by c-Myc. One holds that death arises from a conflict in growth signals which is generated by the inappropriate or unscheduled expression of c-Myc under conditions that would normally promote growth arrest. In this 'Conflict' model, induction of apoptosis is not a normal function of c-Myc but a pathological manifestation of its deregulation. It thus has significance only for models of carcinogenic progression in which myc genes are invariably disrupted.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed1995

Proliferating cell nuclear antigen (PCNA) immunostaining--a prognostic factor in ovarian cancer?

The measurement of tumour cell proliferation is becoming increasingly recognised in defining prognostic groups. Proliferating cell nuclear antigen (PCNA) immunolocalisation can be used as an index of cell proliferation and may define the extent of departure from normal growth control. The monoclonal antibody PC10 stains PCNA in archival paraffin-embedded tissue. This study investigates its potential as a prognostic marker in early and advanced ovarian cancer. A three-stage immunoperoxidase technique was developed to detect the monoclonal antibody PC10. Archival paraffin-embedded tissue from 19 stage I ovarian tumours (13 malignant and six borderline) and 79 advanced (stage IIb-IV) ovarian tumours (patients entered into the Third North-West Thames Ovarian Cancer Trial) was immunostained with PC10. PC10 immunostaining was performed successfully in 91.8% of cases. The PC10 labelling index (PC10 LI) ranged from 1.5% to 88% with a mean value of 47.4%. Stage I borderline tumours had significantly lower PCNA labelling indexes than stage I malignant tumours (P < 0.048). In advanced disease there was an inverse correlation between PC10 and overall survival, and in those patients who underwent good debulking surgery (37 patients with disease < 2 cm diameter) a low PC10 value (< 36.5%) correlated with improved survival (log-rank trend test for survival, chi 2 = 5.75, P = 0.017). PCNA immunostaining defines a good prognostic subgroup in adequately debulked patients with ovarian cancer.

Adult↗

PubMed1976

Cell proliferation in the descending colon of dimethylhydrazine treated rats and in dimethylhydrazine induced adenocarcinomata.

A stathmokinetic technique which has estimable precision has been used to estimate mitotic rates in the crypts of Lieberkühn in the descending colon of normal, and of dimethylhydrazine (DMH)-treated rats, as well as in DMH-induced adenocarcinomata. Estimates of the mean number of proliferating and of non-proliferating cells per crypt of Lieberkühn were also made in normal and in DMH-treated rats. In normal rats, epithelial cell proliferation was found to be relatively slow in the basal one-fifth of the crypts of Lieberkühn and to be most rapid in the second one-fifth of the crypt. In DMH-treated rats the number of cells around the circumference of transversely sectioned crypts was significantly increased, as was the number of proliferating cells present in longitudinally sectioned crypts. The region of relatively slow cell proliferation in the base of the crypts was expanded to occupy the lower two-fifths of the crypt in DMH-treated rats whilst the region of most rapid cell proliferation was displaced upwards to occupy the third one-fifth of the crypt. In DMH-induced adenocarcinomata cell proliferation occurred at a rate similar to that in the relatively quiescent zone at the bases of the colinic crypts in normal animals. However, tumour cell proliferation was substantially slower than that in the second one-fifth of the crypt in normal animals.

Adenocarcinoma↗

PubMed2024

Transient Zn2+ deficiency induces replication stress and compromises daughter cell proliferation.

Cells must replicate their genome quickly and accurately, and they require metabolites and cofactors to do so. Ionic zinc (Zn2+) is an essential micronutrient that is required for hundreds of cellular processes, including DNA synthesis and adequate proliferation. Deficiency in this micronutrient impairs DNA synthesis and inhibits proliferation, but the mechanism is unknown. Using fluorescent reporters to track single cells via long-term live-cell imaging, we find that Zn2+ is required at the G1/S transition and during S phase for timely completion of S phase. A short pulse of Zn2+ deficiency impairs DNA synthesis and increases markers of replication stress. These markers of replication stress are reversed upon resupply of Zn2+. Finally, we find that if Zn2+ is chelated during the mother cell's S phase, daughter cells enter a transient quiescent state, maintained by sustained expression of p21, which disappears upon reentry into the cell cycle. In summary, short pulses of mild Zn2+ deficiency in S phase specifically induce replication stress, which causes downstream proliferation impairments in daughter cells.

Zinc↗

PubMed2004

[Effects of steep pulsed electric fields on cancer cell proliferation and cell cycle].

To assess study the cytocidal and inhibitory effects of steep pulsed electric fields (SPEFs) on ovarian cancer cell line SKOV3, the cancer cell suspension was treated by SPEFs with different parameters (frequency, pulse duration, peak value of voltage). Viability rate and growth curves of two test groups (high dosage and low dosage of SPEFs) and one control group were also measured. The DNA contents and cell cycle were analyzed by flow cytometry (FCM). Different dosing levels of SPEFs exerted obviously different effects on cancer cell viability. With the enhancement of each pulse parameter, the viability rate was promoted and the inhibitory effect on the proliferation of treated cells was more evident. The cells exposed to SPEFs grew slower than the control. The ratio of S+G2/M phase cells was decreased, which restrained the DNA synthesis and division, but the ratio of G0/G1 phase cells was increased in the treated groups. It was also indicated that the SPEFs blocked the cell transition from G0/G1 phase to S+G2/M phase. There was a significant difference in cell cycle between treated group and control group (P<0.01). Lethal effects of SPEFs were represented by inhibiting the cancer cell proliferation at the cell level and by influencing the cell cycle at the DNA level.

Adenocarcinoma↗