MicroRNA-196b inhibits late apoptosis of pancreatic cancer cells by targeting CADM1

Wang, Hongling; Zhou, Rui; Liu, Jing; Chang, Ying; Shi, Liu; Wang, Xiaobing; Huang, Meifang; Zhao, Qiu

doi:10.1038/s41598-017-11248-3

Cited by 24 publications

(11 citation statements)

References 28 publications

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“…Moreover, our findings also exhibited a close relation between miR-196b expression and the pathological characteristics and prognosis of LSCC patients. Similar in pancreatic cancer, miR-196b was also positively associated with poor differentiation, tumor size, lymphatic invasion and TNM staging [37], and a high expression of miR-196b predicted a lower overall survival rate than those with a low expression in pediatric acute myeloid leukemia [11], further highlighting the promoting role of miR-196b in LSCC.…”

Section: Discussionmentioning

confidence: 99%

MiR-196b affects the progression and prognosis of human LSCC through targeting PCDH-17

Luo

Sun

2019

Auris Nasus Larynx

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Section: Discussionmentioning

confidence: 99%

MiR-196b affects the progression and prognosis of human LSCC through targeting PCDH-17

Luo

Sun

2019

Auris Nasus Larynx

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“…Catuogno et al (28) showed that miR-34c protected lung cancer cells from paclitaxel-induced apoptosis. Wang et al (29) reported that miR-196b inhibited late apoptosis in pancreatic cancer cells. Cao et al (30) reported that overexpression of miR-196b enhanced viability and inhibited apoptosis of human HeLa and 293T cells.…”

Section: Role Of Lncrna Loc105374325 In Podocytes Of Fsgsmentioning

confidence: 99%

The long noncoding RNA LOC105374325 causes podocyte injury in individuals with focal segmental glomerulosclerosis

Zhou

Han

Shi

et al. 2018

Journal of Biological Chemistry

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Focal segmental glomerulosclerosis (FSGS) is a common kidney disease that results in nephrotic syndrome. FSGS arises from dysfunction and apoptosis of podocytes in the glomerulus of the kidney, leading to podocytopathy. The molecular mechanisms underlying podocyte apoptosis remain incompletely understood. Using an array of gene expression profiling, PCR, and in situ hybridization assay, we found here that the levels of the long noncoding RNA LOC105374325 were elevated in the renal podocytes of individuals with FSGS. We also observed that the microRNAs miR-34c and miR-196a/b down-regulated the expression of the apoptosis regulators BCL2-associated X, apoptosis regulator (Bax), and BCL2 antagonist/killer 1 (Bak) in podocytes. Competitive binding between LOC105374325 and miR-34c or miR-196a/b increased Bax and Bak levels and caused podocyte apoptosis. Of note, the mitogen-activated protein kinase P38 and the transcription factor CCAAT enhancer-binding protein ␤ (C/EBP␤) up-regulated LOC105374325 expression. P38 inhibition or C/EBP␤ silencing decreased LOC105374325 levels and inhibited apoptosis in adriamycin-treated podocytes. LOC105374325 overexpression decreased miR-34c and miR-196a/b levels, increased Bax and Bak levels, and induced proteinuria and focal segmental lesions in mice. In conclusion, activation of the P38/C/ EBP␤ pathway stimulates the expression of LOC105374325, which, in turn, increases Bax and Bak levels and causes apoptosis by competitively binding to miR-34c and miR-196a/b in the podocytes of individuals with FSGS.

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“…This is not the first time that miRNA has selectively affected the late-stage apoptosis of cancer cells. A previous study by Wang et al demonstrated that miRNA-196b promoted pancreatic cancer cell growth by inhibiting late apoptosis via negative regulation of CADM1 expression (66). Further studies are required to investigate the molecular mechanism of how miR-182 mediates late apoptosis in GIST cells.…”

Section: Discussionmentioning

confidence: 97%

miR-182 controls cell growth in gastrointestinal stromal tumors by negatively regulating CYLD expression

Ling

Cao

2018

Oncol Rep

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Gastrointestinal stromal tumors (GISTs) are the most common type of mesenchymal tumor of the digestive tract. MicroRNAs (miRNAs) are short non-coding RNAs, which control gene expression at a post-transcriptional level. Dysregulated miRNAs are involved in various types of human disease, including cancer. In the present study, it was revealed that miRNA-182 (miR-182) expression was significantly upregulated in human GISTs compared with adjacent normal tissues. Overexpression of miR-182 enhanced GIST-T1 cell growth, with increased proliferation and decreased apoptosis. miR-182 upregulation also promoted colony formation and migration of GIST-T1 cells. In addition, cylindromatosis (CYLD) was identified as a direct target of miR-182. Overexpression of miR-182 suppressed CYLD expression and enhanced downstream nuclear factor (NF)-κB activation. It was also determined that the expression of CYLD was downregulated in association with upregulated miR-182 in human GISTs. In conclusion, these results demonstrated that miR-182 promoted GIST cell growth by negatively regulating CYLD expression. These findings indicated that miR-182 antagonist may be a promising therapeutic strategy for the treatment of human GIST.

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MicroRNA-196b inhibits late apoptosis of pancreatic cancer cells by targeting CADM1

Cited by 24 publications

References 28 publications

MiR-196b affects the progression and prognosis of human LSCC through targeting PCDH-17

MiR-196b affects the progression and prognosis of human LSCC through targeting PCDH-17

The long noncoding RNA LOC105374325 causes podocyte injury in individuals with focal segmental glomerulosclerosis

miR-182 controls cell growth in gastrointestinal stromal tumors by negatively regulating CYLD expression

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