scholarly journals Scutellarein Induces Fas-Mediated Extrinsic Apoptosis and G2/M Cell Cycle Arrest in Hep3B Hepatocellular Carcinoma Cells

Nutrients ◽  
2019 ◽  
Vol 11 (2) ◽  
pp. 263 ◽  
Author(s):  
Ha Sang Eun ◽  
Kim Seong Min ◽  
Lee Ho Jeong ◽  
Preethi Vetrivel ◽  
Venu Venkatarame Gowda Saralamma ◽  
...  
Keyword(s):  
Hepatocellular Carcinoma ◽  
Cell Cycle ◽  
Cell Cycle Arrest ◽  
Fas Ligand ◽  
Biological Activities ◽  
Cyclin B1 ◽  
Phase Cell ◽  
Cycle Arrest ◽  
Wide Range ◽  
Hep3b Cells

Scutellarein (SCU), a flavone found in the perennial herb Scutellaria baicalensis, is known for a wide range of biological activities. In the present study, we investigated the effects of treatment with SCU flavonoids on inducing apoptosis via the extrinsic pathway in Hep3B cells. SCU treatment significantly inhibited Hep3B cell proliferation and induced G2/M phase cell cycle arrest by inhibiting the expression levels of the proteins Cdc25C, cdk1 and Cyclin B1. Allophycocyanin (APC)/Annexin V and propidium iodide (PI) double-staining showed upregulation of apoptotic cell death fraction. We further confirmed apoptosis by 4′-6-diamidino-2-phenylindole (DAPI) fluorescent staining and observed DNA fragmentation with agarose gel electrophoresis. Further, immunoblotting results showed that treatment with SCU showed no changes in Bax and Bcl-xL protein levels. In addition, SCU treatment did not affect the mitochondrial membrane potential in Hep3B cells. On the contrary, treatment with SCU increased the expression of Fas and Fas ligand (FasL), which activated cleaved caspase-8, caspase-3, and polymeric adenosine diphosphate ribose (PARP), whereas the expression level of death receptor 4 (DR4) decreased. We confirmed that the proteins expressed upon treatment with SCU were involved in the Fas-mediated pathway of apoptosis in Hep3B cells. Thus, our findings in the current study strongly imply that SCU can be a basic natural source for developing potent anti-cancer agents for hepatocellular carcinoma (HCC) treatment.

scholarly journals The Novel Nature Microtubule Inhibitor Ivalin Induces G2/M Arrest and Apoptosis in Human Hepatocellular Carcinoma SMMC-7721 Cells In Vitro

Medicina ◽  
2019 ◽  
Vol 55 (8) ◽  
pp. 470 ◽  
Author(s):  
Fangyuan Liu ◽  
Shiqi Lin ◽  
Caiyun Zhang ◽  
Jiahui Ma ◽  
Zhuo Han ◽  
...  
Keyword(s):  
Hepatocellular Carcinoma ◽  
Cell Cycle ◽  
Cell Cycle Arrest ◽  
Western Blotting ◽  
Network Formation ◽  
Cyclin B1 ◽  
Human Hepatocellular Carcinoma ◽  
Microtubule Depolymerization ◽  
Microtubule Network ◽  
Cycle Arrest

Background and Objectives: Microtubules are an attractive target for cancer chemotherapy. Previously, we reported that Ivalin exhibited excellent anti-migration and anti-invasion activities in human breast cancer cells. Here, we examined the microtubule inhibition effect of Ivalin in human hepatocellular carcinoma SMMC-7721 cells. Materials and Methods: We used the 3-(4,5-dimethylthiazol)-2,5-diphenyltetrazolium bromide (MTT) assay to evaluate the cell proliferation effect of Ivalin and flow cytometry analysis to detect the apoptotic and cell cycle arrest effects of Ivalin. Immunofluorescence staining was used to measure the effect of Ivalin on the cytoskeleton network, and Western blotting was used to detect the expression levels of Bax, Bcl-2, Cdc2, phosphor-Cdc2, Cdc25A, Cyclin B1, and tubulin. Results: Ivalin induced cell cycle G2/M arrest and subsequent triggered apoptosis in human hepatocellular carcinoma SMMC-7721 cells. Furthermore, microtubules were shown to be involved in Ivalin-meditated apoptosis. In this connection, Ivalin treatment suppressed cellular microtubule network formation by regulating microtubule depolymerization. Moreover, Western blotting revealed Cdc25A and Cyclin B1 were upregulated in Ivalin-meditated cell cycle arrest. Subsequently, the induction of Bax (a proapoptotic protein) and reduction of Bcl-2 (an anti-apoptotic protein) expression were observed in Ivalin-treated SMMC-7721 cells. Conclusion: Ivalin induced microtubule depolymerization, then blocked cells in mitotic phase, and eventually resulted in apoptosis in SMMC-7721 cells. Collectively, these data indicate that Ivalin, acting as a novel inhibitor of microtubules, could be considered as a promising lead in anticancer drug development.

scholarly journals Ghrelin enhances cisplatin sensitivity in HO-8910 PM human ovarian cancer cells

2021 ◽  
Vol 14 (1) ◽  
Author(s):  
Yun Leng ◽  
Can Zhao ◽  
Guoliang Yan ◽  
Shuangyue Xu ◽  
Yinggui Yang ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Ovarian Cancer ◽  
Cell Cycle Arrest ◽  
Cyclin B1 ◽  
Inhibitory Effect ◽  
S Phase ◽  
Phase Cell ◽  
Ovarian Cancer Cells ◽  
Cycle Arrest

Abstract Background Resistance to platinum-based chemotherapy is one of the crucial problems in ovarian cancer treatment. Ghrelin, a widely distributed peptide hormone, participates in a series of cancer progression. The aim of this study is to determine whether ghrelin influences the sensitivity of ovarian cancer to cisplatin, and to demonstrate the underlying mechanism. Methods The anti-tumor effects of ghrelin and cisplatin were evaluated with human ovarian cancer cells HO-8910 PM in vitro or in vivo. Cell apoptosis and cell cycle were analyzed via flow cytometry assay. The signaling pathway and the expression of cell cycle protein were analyzed with Western Blot. Results Our results showed that treatment with ghrelin specifically inhibited cell proliferation of HO-8910 PM and sensitized these cells to cisplatin via S phase cell cycle arrest, and enhanced the inhibitory effect of cisplatin on tumor growth of HO-8910 PM derived xenografts in vivo. Treatment with ghrelin inhibited the expression of p-Erk1/2 and p-p38, which was opposite the effect of cisplatin. However, under the treatment of ghrelin, cisplatin treatment exhibited a stronger effect on inhibiting P21 expression, upregulating p-CDK1 and cyclin B1 expression, and blocking cell cycle progression. Mechanistically, ghrelin promoted S phase cell cycle arrest and upregulated p-CDK1 and cyclin B1 expression induced by cisplatin via inhibition of p38. Conclusion This study revealed a specifically inhibitory effect of ghrelin on platinum-resistance via suppressing p-P38 and subsequently promoting p-CDK1 mediated cell cycle arrest in HO-8910 PM.

scholarly journals Toona SinensisandMoschusDecoction Induced Cell Cycle Arrest in Human Cervical Carcinoma HeLa Cells

2014 ◽  
Vol 2014 ◽  
pp. 1-8 ◽  
Author(s):  
Hong Zhen ◽  
Yifei Zhang ◽  
Zhijia Fang ◽  
Zhiwei Huang ◽  
Chongge You ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Cell Cycle Arrest ◽  
Hela Cells ◽  
Biological Activities ◽  
S Phase ◽  
Phase Cell ◽  
Mrna Levels ◽  
Cyclin E1 ◽  
Toona Sinensis ◽  
Cycle Arrest

Toona sinensisandMoschusare two herb materials used in traditional Chinese medicine, most commonly for their various biological activities. In this study, we investigated the inhibitory effect of three decoctions fromToona sinensis,Moschus,andToona sinensisandMoschusin combination on cell growth in several normal and cancer cell lines by cell viability assay. The results showed that the combined decoction exhibited the strongest anticancer effects, compared to two single decoctions. The observations indicated that the combined decoction did not induce cell apoptosis and autophagy in HeLa cells by fluorescence microscopy. Flow cytometry analysis revealed that the combined decoction arrested HeLa cell cycle progression in S-phase. After the decoction incubation, among 41 cell cycle related genes, eight were reduced, while five were increased in mRNA levels by real-time PCR assay. Western blotting showed that there were no apparent changes of protein levels of Cyclin E1, while P27 expression significantly declined and the levels of CDC7 and CDK7 obviously increased. The data suggest that the RB pathway is partially responsible for the decoction-induced S-phase cell cycle arrest in HeLa cells. Therefore, the combined decoction may have therapeutic potential as an anticancer formula for certain cancers.

scholarly journals Incaspitolide A extracted from Carpesium cernuum induces apoptosis in vitro via the PI3K/AKT pathway in benign prostatic hyperplasia

2021 ◽  
Author(s):  
Xiaoyue Chen ◽  
Jingrui Song ◽  
Dongbo Yuan ◽  
Qing Rao ◽  
Kehua Jiang ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Cell Proliferation ◽  
Benign Prostatic Hyperplasia ◽  
Cell Cycle Arrest ◽  
Cyclin B1 ◽  
Prostatic Hyperplasia ◽  
Phase Cell ◽  
Prolonged Treatment ◽  
Akt Pathway ◽  
Cycle Arrest

Benign prostatic hyperplasia (BPH) is a common disease that occurs mainly in older men. The pathogenesis of BPH is complex and patients face a prolonged treatment course, and novel drugs with better selectivity and lower toxicity are required. incaspitolide A (compound TMJ-12) is a germacrane-type sesquiterpenoid compound extracted from the plant Carpesium carnuum. Extracts of C. carnuum are known to exert suppressive effects on BPH-1 cells. In this study, we investigated the molecular mechanisms underlying the suppressive effect of TMJ-12 specifically on BPH-1 cells. A cytotoxicity assay indicated that TMJ-12 inhibited BPH-1 cell proliferation, while flow cytometry assays showed that TMJ-12 induced G2/M phase cell cycle arrest and the apoptosis of BPH-1 cells. TMJ-12 was also shown to regulate the expression of several apoptosis- and cell cycle-related proteins, namely Bcl-2, Bax, Bad, Caspase-9, Caspase-3, CDK1, Cyclin B1, CDC25C, and c-Myc, among others. Collapse of the mitochondrial membrane potential (ΔΨm) following exposure to TMJ-12 was detected with the JC-1 staining assay. Further investigation revealed that treatment with TMJ-12 inhibited the PI3K/AKT pathway by increasing the expression of PTEN. Taken together, the results suggest that TMJ-12 prevents BPH-1 cell proliferation via the PI3K/AKT pathway by inducing apoptosis and cell cycle arrest.

Involvement of the role of Chk1 in lithium‐induced G2/M phase cell cycle arrest in hepatocellular carcinoma cells

2008 ◽  
Vol 104 (4) ◽  
pp. 1181-1191 ◽  
Author(s):  
Xiao‐Ming Wang ◽  
Jiao Li ◽  
Xiao‐Cheng Feng ◽  
Qiong Wang ◽  
Dong‐Yin Guan ◽  
...  
Keyword(s):  
Hepatocellular Carcinoma ◽  
Cell Cycle ◽  
Cell Cycle Arrest ◽  
Carcinoma Cells ◽  
Phase Cell ◽  
Hepatocellular Carcinoma Cells ◽  
Cycle Arrest ◽  
M Phase
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