scholarly journals NFAT c1 is a tumor suppressor in hepatocellular carcinoma and induces tumor cell apoptosis by activating the FasL‐mediated extrinsic signaling pathway

2018 ◽  
Vol 7 (9) ◽  
pp. 4701-4717 ◽  
Author(s):  
Sanrong Xu ◽  
Penghao Shu ◽  
Song Zou ◽  
Xiaofeng Shen ◽  
Yuanqian Qu ◽  
...  
Keyword(s):  
Hepatocellular Carcinoma ◽  
Tumor Suppressor ◽  
Tumor Cell ◽  
Signaling Pathway ◽  
Cell Apoptosis ◽  
Tumor Cell Apoptosis

scholarly journals Sorafenib Blocks the RAF/MEK/ERK Pathway, Inhibits Tumor Angiogenesis, and Induces Tumor Cell Apoptosis in Hepatocellular Carcinoma Model PLC/PRF/5

2006 ◽  
Vol 66 (24) ◽  
pp. 11851-11858 ◽  
Author(s):  
Li Liu ◽  
Yichen Cao ◽  
Charles Chen ◽  
Xiaomei Zhang ◽  
Angela McNabola ◽  
...  
Keyword(s):  
Hepatocellular Carcinoma ◽  
Tumor Cell ◽  
Tumor Angiogenesis ◽  
Cell Apoptosis ◽  
Erk Pathway ◽  
Tumor Cell Apoptosis

scholarly journals SOX30, a novel epigenetic silenced tumor suppressor, promotes tumor cell apoptosis by transcriptional activating p53 in lung cancer

Oncogene ◽  
2014 ◽  
Vol 34 (33) ◽  
pp. 4391-4402 ◽  
Author(s):  
F Han ◽  
W Liu ◽  
X Jiang ◽  
X Shi ◽  
L Yin ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Tumor Suppressor ◽  
Tumor Cell ◽  
Cell Apoptosis ◽  
Tumor Cell Apoptosis

scholarly journals Antitumor Effect of Periplocin in TRAIL-Resistant Human Hepatocellular Carcinoma Cells through Downregulation of IAPs

2013 ◽  
Vol 2013 ◽  
pp. 1-11 ◽  
Author(s):  
Chieh-Fang Cheng ◽  
I-Huang Lu ◽  
Hsiang-Wen Tseng ◽  
Chung-Yuan Sun ◽  
Li-Tsen Lin ◽  
...  
Keyword(s):  
Hepatocellular Carcinoma ◽  
Tumor Growth ◽  
Tumor Cell ◽  
Cell Apoptosis ◽  
Cardiac Glycosides ◽  
Chinese Herb ◽  
Carcinoma Cells ◽  
Root Bark ◽  
Tumor Cell Apoptosis ◽  
Hepatocellular Carcinoma Cells

Cortex periplocae is the dried root bark ofPeriploca sepiumBge., a traditional Chinese herb medicine. It contains high amounts of cardiac glycosides. Several cardiac glycosides have been reported to inhibit tumor growth or induce tumor cell apoptosis. We extracted and purified cortex periplocae and identified periplocin as the active ingredient that inhibited the growth of TNF-related apoptosis-inducing ligand-(TRAIL-) resistant hepatocellular carcinoma cells. The antitumor activity of periplocin was further increased by TRAIL cotreatment. Periplocin sensitized TRAIL-resistant HCC through the following two mechanisms. First, periplocin induced the expression of DR4 and FADD. Second, the cotreatment of TRAIL and periplocin suppressed several inhibitors of apoptosis (IAPs). Both mechanisms resulted in the activation of caspase 3, 8, and 9 and led to cell apoptosis. In addition, intraperitoneal injection (IP) of periplocin repressed the growth of hepatocellular carcinoma (HCC) in xenograft tumor model in mice. In summary, periplocin sensitized TRAIL-resistant HCC cells to TRAIL treatment and resulted in tumor cell apoptosis and the repression of tumor growthin vivo.

Proapoptotic RYBP interacts with FANK1 and induces tumor cell apoptosis through the AP-1 signaling pathway

2016 ◽  
Vol 28 (8) ◽  
pp. 779-787 ◽  
Author(s):  
Wen Ma ◽  
Xuan Zhang ◽  
Meng Li ◽  
Xiaoli Ma ◽  
Bingren Huang ◽  
...  
Keyword(s):  
Tumor Cell ◽  
Signaling Pathway ◽  
Cell Apoptosis ◽  
Tumor Cell Apoptosis

FOXD3, frequently methylated in colorectal cancer, acts as a tumor suppressor and induces tumor cell apoptosis under ER stress via p53

2019 ◽  
Vol 41 (9) ◽  
pp. 1253-1262 ◽  
Author(s):  
Ming Xu ◽  
Jing Zhu ◽  
Shuiping Liu ◽  
Chan Wang ◽  
Qinglan Shi ◽  
...  
Keyword(s):  
Colorectal Cancer ◽  
Tumor Suppressor ◽  
Tumor Cell ◽  
Er Stress ◽  
Cell Lines ◽  
Cell Apoptosis ◽  
Primary Tumors ◽  
Tumor Cell Apoptosis ◽  
Specific Pcr ◽  
Forkhead Box

Abstract Forkhead box D3 (FOXD3), an important member of the forkhead box transcription factor family, has many biological functions. However, the role and signaling pathways of FOXD3 in colorectal cancer (CRC) are still unclear. We examined FOXD3 expression and methylation in normal colon mucosa, CRC cell lines and primary tumors by reverse transcription–polymerase chain reaction, methylation-specific PCR and bisulfite genomic sequencing. We also evaluated its tumor-suppressive function by examining its modulation of apoptosis under endoplasmic reticulum (ER) stress in CRC cells. The FOXD3 target signal pathway was identified by western blotting, immunofluorescence and chromatin immunoprecipitation. We found that FOXD3 was frequently methylated and silenced in CRC cell lines and was downregulated in CRC tissues compared with paired adjacent non-tumor tissues. Meanwhile, low FOXD3 protein expression was significantly correlated with poor histopathological grading, lymph node metastasis and poor prognosis of patients, indicating its potential as a tumor marker that may be of potential value as a therapeutic target for CRC. Moreover, restoration of FOXD3 expression inhibited the proliferation and migration of tumor cells. FOXD3 also increased mitochondrial apoptosis through the unfolded protein response under ER stress. Furthermore, we found that FOXD3 could bind directly to the promoter of p53 and enhance its expression. Knockdown of p53 impaired the effect of apoptosis induced by FOXD3. In conclusion, we showed for the first time that FOXD3, which is frequently methylated in CRC, acted as a tumor suppressor inducing tumor cell apoptosis under ER stress via p53.

scholarly journals Jianpi-Huayu Formula Inhibits Development of Hepatocellular Carcinoma by Regulating Expression of miR-602, Which Targets the RASSF1A Gene

2020 ◽  
Vol 19 ◽  
pp. 153473541990080 ◽  
Author(s):  
Yajing Huang ◽  
Cheng Zhou ◽  
Huihong Wen ◽  
Yongxu Chen ◽  
Yingjie Xie ◽  
...  
Keyword(s):  
Hepatocellular Carcinoma ◽  
Protein Expression ◽  
Tumor Cell ◽  
Liver Tumor ◽  
Cell Apoptosis ◽  
Control Group ◽  
Tumor Cell Apoptosis ◽  
Expression Levels ◽  
Rassf1a Gene ◽  
Tumor Tissues

The traditional Chinese medicine formula Jianpi-Huayu (JPHY) has been reported to be effective in the treatment of hepatocellular carcinoma (HCC). However, its underlying mechanism remains unclear. In this article, we employed an orthotopic transplantation model in nude mice to explore whether JPHY could inhibit the development of HCC by regulating miR-602, which targets the Ras association domain-containing protein 1A (RASSF1A) pathway. HCC SMMC-7721 cells were treated with JPHY to test whether the RASSF1A gene as mediated by miR-602 affected the proliferation and apoptosis of tumor cells. We subsequently detected miR-602, RASSF1A, and tumor cell apoptosis–related markers in cells and liver tumor tissues. We observed that mice treated with JPHY had smaller tumors and higher survival rates than untreated ones. Similarly, JPHY-treated SMMC-7721 cells exhibited alterations in morphology and higher cytotoxicity compared with the control group. Furthermore, we found that JPHY decreased overexpression of miR-602 and increased protein expression levels of the RASS1A gene, which in turn altered protein expression levels of tumor cell apoptosis–related genes in the cells and liver tumor tissues of drug-treated mice. These results indicated that JPHY could potentially be used to treat HCC by targeting miR-602, which targets the RASSF1A gene, which in turn plays a major role in HCC pathogenesis.

scholarly journals Engineered neutrophil-derived exosome-like vesicles for targeted cancer therapy

2022 ◽  
Vol 8 (2) ◽  
Author(s):  
Jiahui Zhang ◽  
Cheng Ji ◽  
Hongbo Zhang ◽  
Hui Shi ◽  
Fei Mao ◽  
...  
Keyword(s):  
Cancer Therapy ◽  
Tumor Cell ◽  
Signaling Pathway ◽  
Cell Apoptosis ◽  
Targeted Cancer Therapy ◽  
Tumor Cell Apoptosis ◽  
Cytotoxic Proteins

Neutrophil-derived exosomes induce tumor cell apoptosis by delivering cytotoxic proteins and activating caspase signaling pathway.

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