MiR-421 Regulates Apoptosis of BGC-823 Gastric Cancer Cells by Targeting Caspase-3

Wu, Jianhong; Yao, Yongliang; Gu, Tao; Wang, Zeyou; Pu, Xia; Sun, Wei; Zhang, Xian; Jiang, Yi-Biao; Wang, Jianjun

doi:10.7314/apjcp.2014.15.13.5463

Cited by 43 publications

(35 citation statements)

References 32 publications

(30 reference statements)

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“…Also, as a terminal enzyme during cell apoptosis, caspase‐3 could be down‐regulated by miR‐124 mimics, and the intervention of miR‐124 mimics could increase the expression of Bcl‐2 but decrease the expression of Bax . Besides, Bcl‐2 expression can directly prevent cancer cell apoptosis, and up‐regulated Bcl‐2 was seen in cancer cells when the activity of Notch signaling pathway was increased . Moreover, miR‐421 could inhibit GC cell apoptosis by suppressing the expression of caspase‐3.41…”

Section: Discussionmentioning

confidence: 99%

Retracted: In vivo and in vitro effects of microRNA‐124 on human gastric cancer by targeting JAG1 through the Notch signaling pathway

Xiao

Yang

et al. 2017

J of Cellular Biochemistry

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In this study, we aim to determine the function of miR-124 on gastric cancer (GC) cells and the underlying mechanism that involves jaddeg1 (JAG1) and the Notch signaling pathway. GC tissues and adjacent tissues from 100 patients suffering from GC were selected. GC SGC-7901 and AGS cells were selected and grouped into control, mimic-NC, miR-124 mimic, inhibitor-NC, miR-124 inhibitor, and miR-124 inhibitor + si-JAG1 groups. RT-qPCR and a Western blotting assay were conducted to detect the expression of miR-124, JAG1, and Notch signaling pathway-related proteins (NICD, HES1, and HES5). MTS, wound-healing, transwell assay and flow cytometry were performed to detect cell proliferation, migration, invasion, cell cycle distribution, and apoptosis, respectively. Compared with adjacent tissues, a lower miR-124 expression and higher JAG1 expression were found in GC tissues. JAG1 is a direct target gene of miR-124. Compared with the control group, the expression of JAG1, NICD, HES1, and HES5, cell invasion, migration, and proliferation in the miR-124 mimic group were decreased, while the apoptosis rate was increased and cells were arrested at the G0/G1 phase. Compared with the miR-124 inhibitor group, the expression of JAG1, NICD, HES1, and HES5, cell invasion, migration, and proliferation in the miR-124 inhibitor + si-JAG1 group were decreased, while the apoptosis rate and cell ratio at the G0/G1 phase were increased. The demonstration that miR-124 inhibits GC cell growth supports the concept that miR-124 functions as a tumor suppressor by a mechanism that involves translational repression of the JAG1 and the inhibition of Notch signaling pathway.

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Section: Discussionmentioning

confidence: 99%

Retracted: In vivo and in vitro effects of microRNA‐124 on human gastric cancer by targeting JAG1 through the Notch signaling pathway

Xiao

Yang

et al. 2017

J of Cellular Biochemistry

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“…For instance, miR-421 may promote the development of neuroblastoma by targeting the tumor suppressor Menin (24). Wu et al (25) observed that miR-421 regulated cellular apoptosis in the undifferentiated gastric cancer cell line BGC-823 by targeting Caspase-3, and thus may be a novel diagnostic biomarker in gastric cancer (26). Analogous to previous results, the present study identified a potential relationship between elevated miR-421 expression and the development of gastric cancer, as indicated by the significant upregulation in miR-421 in patients presenting with lymph node metastasis and/or higher clinical stages of gastric cancer (III/IV).…”

Section: Discussionmentioning

confidence: 99%

MicroRNA-421 promotes the proliferation and metastasis of gastric cancer cells by targeting claudin-11

Yang

Mei

Liu

et al. 2017

Experimental and Therapeutic Medicine

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Abstract. The present study aimed to evaluate the expression of microRNA (miR)-421 in gastric cancer and to investigate its biological function and underlying mechanism of action in the development of gastric cancer. The expression of miR-421 was measured in 60 pairs of clinically removed gastric cancer tissues and matched adjacent normal gastric tissues by reverse transcription-quantitative polymerase chain reaction. In addition, following transfection with an miR-421 inhibitor to suppress the expression of miR-421, the proliferation, migration and cell cycle distribution of human gastric carcinoma MKN28/MKN74 cells were determined by cell counting, Transwell and flow cytometry assays. The target gene of miR-421 was also predicted using bioinformatic analysis and verified by dual-luciferase reporter gene assay and western blot analysis. Furthermore, overexpression of the miR-421 target protein was induced in MKN28/MKN74 cells to determine its function. It was observed that miR-421 was significantly upregulated in gastric cancer tissues and that the expression of miR-421 was associated with lymph node metastasis and the clinical stage of gastric cancer (all P<0.05). Claudin11 (CLDN11) was predicted and verified as a direct target of miR-421. In vitro experiments demonstrated that inhibition of miR-421 expression suppressed the proliferation and metastasis of MKN28/MKN74 cells and induced G1/S-phase cell cycle arrest (all P<0.05). Analagous results were observed in MKN28/MKN74 cells following overexpression of the CLDN11 protein. Collectively, these data suggest that miR-421 may promote the proliferation, invasion and metastasis of gastric cancer by inhibiting the expression of CLDN11.

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“…The downregulation of miR-23a increased the 5-FU-induced apoptosis in colon cancer cells [179]. Wu et al (2014) [181] displayed that miR-421 upregulated in human gastric cell lines and tissues. miR-421 downregulated the expression of caspase-3 and blocked the apoptosis of cancer cells.…”

Section: Micrornas In Extrinsic and Intrinsic Apoptotic Pathwaysmentioning

confidence: 98%

Major apoptotic mechanisms and genes involved in apoptosis

et al. 2016

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As much as the cellular viability is important for the living organisms, the elimination of unnecessary or damaged cells has the opposite necessity for the maintenance of homeostasis in tissues, organs and the whole organism. Apoptosis, a type of cell death mechanism, is controlled by the interactions between several molecules and responsible for the elimination of unwanted cells from the body. Apoptosis can be triggered by intrinsically or extrinsically through death signals from the outside of the cell. Any abnormality in apoptosis process can cause various types of diseases from cancer to auto-immune diseases. Different gene families such as caspases, inhibitor of apoptosis proteins, B cell lymphoma (Bcl)-2 family of genes, tumor necrosis factor (TNF) receptor gene superfamily, or p53 gene are involved and/or collaborate in the process of apoptosis. In this review, we discuss the basic features of apoptosis and have focused on the gene families playing critical roles, activation/inactivation mechanisms, upstream/downstream effectors, and signaling pathways in apoptosis on the basis of cancer studies. In addition, novel apoptotic players such as miRNAs and sphingolipid family members in various kind of cancer are discussed.

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MiR-421 Regulates Apoptosis of BGC-823 Gastric Cancer Cells by Targeting Caspase-3

Cited by 43 publications

References 32 publications

Retracted: In vivo and in vitro effects of microRNA‐124 on human gastric cancer by targeting JAG1 through the Notch signaling pathway

Retracted: In vivo and in vitro effects of microRNA‐124 on human gastric cancer by targeting JAG1 through the Notch signaling pathway

MicroRNA-421 promotes the proliferation and metastasis of gastric cancer cells by targeting claudin-11

Major apoptotic mechanisms and genes involved in apoptosis

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