MicroRNA‐374b inhibits cervical cancer cell proliferation and induces apoptosis through the p38/ERK signaling pathway by binding to JAM‐2

Li, Guang‐Cai; Cao, Xiaoyun; Li, Ying-Ni; Qiu, Yu; Liu, Xing‐Jie; Sun, Xiangxiu

doi:10.1002/jcp.26574

Cited by 39 publications

(28 citation statements)

References 28 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Previous studies have reported the downregulation of miR‐374b in pancreatic cancer, cervical cancer and colorectal cancer, which is consistent with our results. Functionally, miR‐374b restrained the progression of liver cancer by inhibiting PD‐1 .…”

Section: Discussionsupporting

confidence: 93%

MicroRNA‐374b mediates the initiation of non‐small cell lung cancer by regulating ITGB1 and p53 expressions

et al. 2020

View full text Add to dashboard Cite

Background: Previous studies have shown that microRNAs (miRNAs) play important roles in the pathogenesis of human cancers. This study aims to clarify the role of miR-374b in non-small cell lung cancer (NSCLC). Methods: In this study, RT-qPCR and western blot analysis were used to measure mRNA and protein expression. The regulatory mechanism of miR-374b/ ITGB1 was investigated by dual-luciferase reporter, CCK-8, and transwell assays. Results: MiR-374b expression was reduced in NSCLC tissues and associated with lymph node metastasis, tumor stage and prognosis in NSCLC patients. Functionally, overexpression of miR-374b inhibited cell viability and metastasis in NSCLC. In addition, miR-374b blocked EMT and promoted p53 expression in NSCLC. MiR-374b was found to directly target ITGB1. Furthermore, upregulation of ITGB1 weakened the antitumor effect of miR-374b in NSCLC. Conclusions: MiR-374b inhibits the tumorigenesis of NSCLC by downregulating ITGB1 and upregulating p53.

show abstract

Section: Discussionsupporting

confidence: 93%

MicroRNA‐374b mediates the initiation of non‐small cell lung cancer by regulating ITGB1 and p53 expressions

et al. 2020

View full text Add to dashboard Cite

show abstract

“…ERK mediated various physiological functions, including proliferation and autophagy 51‐53 . However, the current study showed that ATG regulates ERK phosphorylation.…”

Section: Discussioncontrasting

confidence: 57%

Trehalose reduces bone loss in experimental biliary cirrhosis rats via ERK phosphorylation regulation by enhancing autophagosome formation

Wang

et al. 2020

FASEB j.

View full text Add to dashboard Cite

Bone loss is a severe complication of primary biliary cirrhosis (PBC). Trehalose was intermittently administered in bile duct‐ligated (BDL) male rats, a PBC‐related osteoporosis model, for 4 weeks to reduce osteoporosis. Femoral bones were assessed ex vivo by micro computed tomography (CT) and histomorphometry. The potential mechanisms related to the reduction of osteoporosis were explored by evaluating the effect of trehalose on osteoblast autophagy, osteogenesis, osteoclastogenesis, and ERK phosphorylation. The results demonstrated that trehalose reduced osteoporosis of BDL rats and decreased osteoblast‐mediated osteoclast differentiation by enhancing osteoblast autophagy to regulate osteoprotegerin (OPG) secretion. Hydroxychloroquine (HCQ) increased the expression of OPG and OPG/receptor activator genes for nuclear factor‐κB ligand (RANKL) ratio, and reduced osteoblast‐mediated osteoclastogenesis by inhibiting autophagy flux and inducing autophagosome formation. Furthermore, trehalose increased the phosphorylation of ERK1/2 in MC3T3‐E1 cells, and the ERK inhibitor PD98059 reversed the upregulation of OPG gene and reduction of trehalose‐induced osteoclastogeneis. The treatment with HCQ markedly increased the ERK phosphorylation. The correlation between autophagosome formation and ERK phosphorylation was confirmed in autophagy proteins (ATG) 4B or ATG5‐deficient cells. Thus, trehalose could decrease osteoblast‐mediated osteoclastogenesis and reduce PBC‐related bone loss by regulating ERK phosphorylation via autophagosome formation.

show abstract

“…Several previous studies have demonstrated that some miRNAs are dysregulated in many cancers, especially in CC . For example, miR‐374b inhibited cell proliferation and induces apoptosis through the p38/ERK signaling pathway by binding to JAM‐2 in cervical cancer . In addition, miR‐136 inhibited proliferation and promoted apoptosis and radiosensitivity of cervical carcinoma through the nuclear factor kappa B (NF‐κB) pathway by targeting E2F1 .…”

Section: Introductionmentioning

confidence: 99%

DANCR‐mediated microRNA‐665 regulates proliferation and metastasis of cervical cancer through the ERK/SMAD pathway

et al. 2019

View full text Add to dashboard Cite

Emerging evidence has indicated that microRNAs (miRNAs) play an important role in cervical cancer (CC). However, the role of miRNA (miR)‐665 in cervical cancer remains unclear. The aim of the present study was to investigate the potential functions of miR‐665 in CC and to identify the underlying mechanisms of action. Herein, we show that miR‐665 was downregulated in CC tissues and cell lines, which is negatively correlated with tumor size, distant metastasis, advanced TNM stage and poor prognosis. Functionally, miR‐665 inhibited cell proliferation, migration and invasion and resistance of cisplatin for CC cells, as well as tumor growth. We validated that transforming growth factor beta receptor 1 (TGFBR1) was a direct target of miR‐665 and mediated the ERK/SMAD pathway. In addition, we identified miR‐665 as the competing endogenous RNA for long noncoding (lnc)‐DANCR. These observations suggested that lnc‐DANCR‐mediated miR‐665 downregulation regulates the malignant phenotype of CC cells by targeting TGFBR1 through the ERK/SMAD pathway, which may present a pathway for novel therapeutic stratagems for CC therapy.

show abstract

MicroRNA‐374b inhibits cervical cancer cell proliferation and induces apoptosis through the p38/ERK signaling pathway by binding to JAM‐2

Cited by 39 publications

References 28 publications

MicroRNA‐374b mediates the initiation of non‐small cell lung cancer by regulating ITGB1 and p53 expressions

MicroRNA‐374b mediates the initiation of non‐small cell lung cancer by regulating ITGB1 and p53 expressions

Trehalose reduces bone loss in experimental biliary cirrhosis rats via ERK phosphorylation regulation by enhancing autophagosome formation

DANCR‐mediated microRNA‐665 regulates proliferation and metastasis of cervical cancer through the ERK/SMAD pathway

Contact Info

Product

Resources

About