scholarly journals Curcumin Inhibits ERK/c-Jun Expressions and Phosphorylation against Endometrial Carcinoma

2019 ◽  
Vol 2019 ◽  
pp. 1-13 ◽  
Author(s):  
Zhenxue Zhang ◽  
Pengfei Yi ◽  
Changchun Tu ◽  
Jiejie Zhan ◽  
Liping Jiang ◽  
...  
Keyword(s):  
Endometrial Carcinoma ◽  
Signaling Pathway ◽  
Inhibitory Effect ◽  
S Phase ◽  
Carcinoma Cells ◽  
Network Pharmacology ◽  
Cycle Arrest ◽  
Anticancer Effects ◽  
Ishikawa Cells

Curcumin has been shown to have anticancer effects in a variety of tumors. However, there are fewer studies on the role of curcumin in endometrial carcinoma (EC). The purpose of this experiment was to examine the inhibitory effect of curcumin on endometrial carcinoma cells and ERK/c-Jun signaling pathway. We first predicted the mechanism of action of curcumin on endometrial carcinoma by network pharmacology. Then, we found that curcumin can decrease the cell viability of Ishikawa cells, inhibit the migration of cancer cells, induce apoptosis, and cause cell cycle arrest in the S phase. For molecular mechanism, curcumin reduced the mRNA expression levels of ERK2 and JUN genes and inhibited the phosphorylation of ERK and c-Jun. This suggests that curcumin inhibits the proliferation of endometrial carcinoma cells by downregulating ERK/c-Jun signaling pathway activity.

Biological role of AKT, and regulation of AKT signaling pathway by thymoquinone: perspectives in cancer therapeutics

2020 ◽  
Vol 20 ◽  
Author(s):  
Md. Junaid ◽  
Yeasmin Akter ◽  
Syeda Samira Afrose ◽  
Mousumi Tania ◽  
Md. Asaduzzaman Khan
Keyword(s):  
Clinical Trials ◽  
Signaling Pathways ◽  
Signaling Pathway ◽  
Inhibitory Effect ◽  
Akt Signaling ◽  
Review Article ◽  
Therapeutic Drug ◽  
Akt Signaling Pathway ◽  
Anti Cancer

Background: AKT/PKB is an important enzyme with numerous biological functions, and its overexpression is related to the carcinogenesis. AKT stimulates different signaling pathways that are downstream of activated tyrosine kinases and phosphatidylinositol 3-kinase, hence functions as an important target for anti-cancer drugs. Objective: In this review article, we have interpreted the role of AKT signaling pathways in cancer and natural inhibitory effect of Thymoquinone (TQ) in AKT and its possible mechanism. Method: We have collected the updated information and data on AKT, their role in cancer and inhibitory effect of TQ in AKT signaling pathway from google scholar, PubMed, Web of Science, Elsevier, Scopus and many more. Results: There are many drugs already developed, which can target AKT, but very few among them have passed clinical trials. TQ is a natural compound, mainly found in black cumin, which has been found to have potential anti-cancer activities. TQ targets numerous signaling pathways, including AKT, in different cancers. In fact, many studies revealed that AKT is one of the major targets of TQ. The preclinical success of TQ suggests its clinical studies on cancer. Conclusion: This review article summarizes the role of AKT in carcinogenesis, its potent inhibitors in clinical trials, and how TQ acts as an inhibitor of AKT and TQ’s future as a cancer therapeutic drug.

Involvement of the p38 MAPK signaling pathway in S-phase cell-cycle arrest induced by Furazolidone in human hepatoma G2 cells

2012 ◽  
Vol 33 (12) ◽  
pp. 1500-1505 ◽  
Author(s):  
Yu Sun ◽  
Shusheng Tang ◽  
Xi Jin ◽  
Chaoming Zhang ◽  
Wenxia Zhao ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Cell Cycle Arrest ◽  
Signaling Pathway ◽  
P38 Mapk ◽  
Mapk Signaling ◽  
S Phase ◽  
Mapk Signaling Pathway ◽  
Phase Cell ◽  
Human Hepatoma ◽  
Cycle Arrest

Role of Estrogen and Estrogen-Related Growth Factor in the Mechanism of Hormone Dependency of Endometrial Carcinoma Cells

Oncology ◽  
1998 ◽  
Vol 55 (1) ◽  
pp. 35-44 ◽  
Author(s):  
Hiroki Hata ◽  
Mieko Hamano ◽  
Jun Watanabe ◽  
Hiroyuki Kuramoto
Keyword(s):  
Growth Factor ◽  
Endometrial Carcinoma ◽  
Carcinoma Cells ◽  
Hormone Dependency

scholarly journals The p53/miR-34a/SIRT1 Positive Feedback Loop in Quercetin-Induced Apoptosis

2015 ◽  
Vol 35 (6) ◽  
pp. 2192-2202 ◽  
Author(s):  
Guohua Lou ◽  
Yanning Liu ◽  
Shanshan Wu ◽  
Jihua Xue ◽  
Fan Yang ◽  
...  
Keyword(s):  
Cell Apoptosis ◽  
Feedback Loop ◽  
Molecular Mechanisms ◽  
Rt Pcr ◽  
Cycle Arrest ◽  
Anticancer Effects ◽  
Huh7 Cells ◽  
Mirnas Expression ◽  
Induced Apoptosis

Background: The anti-tumor effects of quercetin have been reported, but the underlying molecular mechanisms remain to be elucidated. The aim of present study was to explore the role of miRNA in the anticancer effects of quercetin. Methods: The differential miRNAs expression between the HepG2 and Huh7 cells treated by quercetin were detected by microarray. The xCELLigence, Flow cytometry, RT-PCR and Western blot were used to analyze the cell proliferation, cell apoptosis, cell cycle arrest, anti-tumor genes, and protein expression. Results: miR-34a was up-regulated in HepG2 cells treated by quercetin exhibiting wild-type p53. When inhibiting the miR-34a, the sensitivity of the cells to quercetin decreased and the expression of the SIRT1 was up-regulated, but the acetylation of p53 and the expression of some genes related to p53 down-regulated. Conclusion: miR-34a plays an important role in the anti-tumor effects of querctin in HCC, miR-34a may be a tiemolecule between the p53 and SIRT1 and is composed of a p53/miR-34a/SIRT1 signal feedback loop, which could enhance apoptosis signal and significantly promote cell apoptosis.

scholarly journals Autophagy Inhibition Potentiates the Anticancer Effects of a Bendamustine Derivative NL-101 in Acute T Lymphocytic Leukemia

2020 ◽  
Vol 2020 ◽  
pp. 1-12 ◽  
Author(s):  
Hang Gao ◽  
Siyue Lou ◽  
Huanwu Hong ◽  
Qiufu Ge ◽  
Huajun Zhao
Keyword(s):  
Apoptotic Cell ◽  
Single Agent ◽  
Acid Group ◽  
Lymphocytic Leukemia ◽  
Cyclin E1 ◽  
Cycle Arrest ◽  
Anticancer Effects ◽  
Histone Hyperacetylation ◽  
Autophagy Inhibition

Acute T lymphocytic leukemia (T-ALL) is an aggressive hematologic resulting from the malignant transformation of T-cell progenitors. Drug resistance and relapse are major difficulties in the treatment of T-ALL. Here, we report the antitumor potency of NL-101, a compound that combines the nitrogen mustard group of bendamustine with the hydroxamic acid group of vorinostat. We found NL-101 exhibited efficient antiproliferative activity in T-ALL cell lines (IC50 1.59–1.89 μM), accompanied by cell cycle arrest and apoptosis, as evidenced by the increased expression of Cyclin E1, CDK2, and CDK4 proteins and cleavage of PARP. In addition, this bendamustine-derived drug showed both a HDACi effect as demonstrated by histone hyperacetylation and p21 transcription and a DNA-damaging effect as shown by an increase in γ-H2AX. Intriguingly, we found that NL-101-induced autophagy in T-ALL cells through inhibiting Akt-mTOR signaling pathway, as indicated by an increase in LC3-I to LC3-II conversion and decrease of p62. Furthermore, inhibition of autophagy by 3-methyladenine increased apoptotic cell death by NL-101, suggesting a prosurvival role of autophagy. In summary, our finding provides rationale for investigation of NL-101 as a DNA/HDAC dual targeting drug in T-ALL, either as a single agent or in combination with autophagy inhibitors.

scholarly journals Huaier Aqueous Extract Induces Hepatocellular Carcinoma Cells Arrest in S Phase via JNK Signaling Pathway

2015 ◽  
Vol 2015 ◽  
pp. 1-11 ◽  
Author(s):  
Chengshuo Zhang ◽  
Jialin Zhang ◽  
Xin Li ◽  
Ning Sun ◽  
Rui Yu ◽  
...  
Keyword(s):  
Hepatocellular Carcinoma ◽  
Cyclin D1 ◽  
Signaling Pathway ◽  
Aqueous Extract ◽  
Cell Apoptosis ◽  
S Phase ◽  
Carcinoma Cells ◽  
Jnk Signaling ◽  
Hepatocellular Carcinoma Cells ◽  
Jnk Signaling Pathway

Huaier aqueous extract, the main active constituent of Huaier proteoglycan, has antihepatocarcinoma activity in experimental and clinical settings. However, the potential and associated antihepatoma mechanisms of Huaier extract are not yet fully understood. Therefore, in this study, we aimed to elucidate the inhibitory proliferation effect of Huaier extract on apoptosis and cycle of HepG2 and Bel-7402 cells. Our data demonstrated that incubation with Huaier extract resulted in a marked decrease in cell viability dose-dependently. Flow cytometric analysis showed that a 48 h treatment of Huaier extract caused cell apoptosis. Typical apoptotic nucleus alterations were observed with fluorescence microscope after Hoechst staining. Immunoblot analysis further demonstrated that Huaier extract activated caspase 3 and PARP. Additionally, Huaier extract inhibited the activity of p-ERK, p-p38, and p-JNK in terms of MAPK. Furthermore, Huaier extract induced HCC cells arrest in S phase and decreased the cycle related protein expression ofβ-catenin and cyclin D1. Studies with JNK specific inhibitor, SP600125, showed that Huaier extract induced S phase arrest and decreasedβ-catenin and cyclin D1 expression via JNK signaling pathway. In conclusion, we verify that Huaier extract causes cell apoptosis and induces hepatocellular carcinoma cells arrest in S phase via JNK pathway, which advances our understanding on the molecular mechanisms of Huaier extract in hepatocarcinoma management.

scholarly journals RRS1 Promotes Retinoblastoma Cell Proliferation and Invasion via Activating the AKT/mTOR Signaling Pathway

2020 ◽  
Vol 2020 ◽  
pp. 1-10
Author(s):  
Xuejing Yan ◽  
Shen Wu ◽  
Qian Liu ◽  
Jingxue Zhang
Keyword(s):  
Signaling Pathway ◽  
Ribosome Biogenesis ◽  
Regulatory Protein ◽  
Ectopic Expression ◽  
Mtor Signaling ◽  
Mtor Signaling Pathway ◽  
Retinoblastoma Cell ◽  
Cycle Arrest ◽  
Pathway Inhibition

Ribosome biogenesis regulatory protein homolog (RRS1) is a protein required for ribosome biogenesis. Recent studies have identified an oncogenic role of RRS1 in some cancers, whereas the involvement of RRS1 in retinoblastoma (RB) remains to be determined. In this study, we aimed to explore the role of RRS1 in RB. We found that the expression of RRS1 was increased in RB tissues and cells. Lentivirus-mediated RRS1 overexpression promoted the proliferation, growth, and invasion of RB cells. Opposite results were found in RRS1 knockdown cells. In addition, RRS1 silencing induced cell cycle arrest at the G1 phase and apoptosis in RB cells, while RRS1 ectopic expression exhibited the opposite effect. At the molecular level, RRS1 activated the AKT/mTOR signaling pathway, inhibition of which largely blunted the proliferation, growth, and invasion of RB cells. Our study suggests that RRS1 functions as an oncogene in RB through activating the AKT/mTOR signaling pathway.

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