MiR-122-5p inhibits cell migration and invasion in gastric cancer by down-regulating <i>DUSP4</i>

Xu, Xiaofeng; Gao, Feng; Wang, Jianjiang; Lan, Tao; Ye, Jinsong; Ding, Li; Ji, Wei; Chen, Xing

doi:10.1080/15384047.2018.1423925

Cited by 77 publications

(56 citation statements)

References 34 publications

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“…MiR‐181a is elevated in advanced‐stage of epithelial ovarian cancer tissues, it is involved in TGF‐β signaling pathway, and promotes epithelial mesenchymal transition (EMT) and metastasis in vivo of ovarian cancer cells (Parikh et al, ). Hsa‐miR‐122‐5p (miR‐122) has been reported to inhibit maglignant phenotypes in gastric cancer (Xu et al, ), cholangiocarcinoma (Liu et al, ), and hepatocellular carcinoma (Xu et al, ). However, it plays a tumor‐promoting role in clear‐cell renal cell carcinoma (Fan et al, ).…”

Section: Introductionmentioning

confidence: 99%

MiR‐122 inhibits epithelial mesenchymal transition by regulating P4HA1 in ovarian cancer cells

Duan

Dong

Dang

et al. 2018

Cell Biology International

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Ovarian cancer is one of the most common gyneacologic malignancies, with high morbidity and high mortality. Hsa-miR-122-5p (miR-122) has been reported with tumor-suppressing roles in various cancers. In this study, miR-122 was overexpressed in ovarian cancer cells, and phenotypic experiments demonstrated that miR-122 inhibited migration and invasion in SKOV3 and OVCAR3 cells. MiR-122 also suppressed epithelial mesenchymal transition (EMT), evidenced by expression changes of E-cadherin, vimentin, matrix metalloproteinase (MMP)2, and MMP14. Prolyl-4-hydroxylase subunit alpha-1 (P4HA1) was identified as a target of miR-122, and downregulated by miR-122. MiR-122-induced the elevation of migration, invasion, and EMT were recovered by P4HA1. Additionally, miR-122 restrained the tumor metastasis of SKOV3 cells in peritoneal cavity of nude mice. In summary, we demonstrated that miR-122 inhibited migration, invasion, EMT, and metastasis in peritoneal cavity of ovarian cancer cells by targeting P4HA1 for the first time, which shed lights on the discovery of miR-122 and P4HA1 as possible potential diagnostic markers and therapeutic targets for ovarian cancer.

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Section: Introductionmentioning

confidence: 99%

MiR‐122 inhibits epithelial mesenchymal transition by regulating P4HA1 in ovarian cancer cells

Duan

Dong

Dang

et al. 2018

Cell Biology International

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“…In several previous studies, miR-122-5p was downregulated and functioned as a tumor suppressor in various cancers, such as hepatocellular (22), non-small cell lung (23), gallbladder (24), bladder (25) and breast cancer (26) as well as GC (27)(28)(29). However, we clearly revealed that miR-122-5p facilitated tumor progression in AFPGC cells and speculated that the function of miR-122-5p and mechanisms underlying tumor progression may be distinct between AFPGC and non-AFPGC.…”

Section: Discussionmentioning

confidence: 99%

Inhibition of apoptosis by miR‑122‑5p in α‑fetoprotein‑producing gastric cancer

et al. 2019

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α-Fetoprotein (AFP)-producing gastric cancer (AFPGC) is recognized as one of the most aggressive tumors with subsequent poor prognosis compared with common gastric cancer (GC) subtypes. However, the molecular mechanism remains to be elucidated. We previously identified that miR-122-5p could be a useful biomarker in AFPGC patients. We examined herein the biological function of miR-122-5p and the molecular mechanism underlying tumor progression in AFPGC. We used the AFPGC cell line (FU97) and miR-122-5p inhibitor to examine the function of miR-122-5p. Moreover, we investigated the possible targets of miR-122-5p. The expression level of miR-122-5p was significantly increased in the FU97 cell line than in common GC cell lines. Also, suppression of miR-122-5p significantly reduced AFP levels and proliferation in AFPGC through an induction of apoptosis. Western blotting revealed that the expression of anti-apoptotic protein (Bcl-2) was decreased and that of pro-apoptotic protein (caspase-3) was increased in miR-122-5p suppression of FU97. Moreover, we revealed that FOXO3 was an important target of miR-122-5p in AFPGC, which inhibited apoptosis and subsequently manifested aggressiveness. In conclusion, miR-122-5p inhibited apoptosis and facilitated tumor progression by targeting FOXO3 in AFPGC, which indicates the possibility of miR-122-5p as a potential therapeutic target in AFPGC.

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“…MiR‐33b‐3p regulated cisplatin sensitivity in cancer cells, possibly by impairing the DNA damage response (Xu et al, ). MiR‐122‐5p inhibited the migration and invasion of gastric cancer cells by inhibiting DUSP4 (Xu et al, ). However, the mechanism of action of these microRNAs in CML requires further exploration and experimental validation.…”

Section: Discussionmentioning

confidence: 99%

Identification of key candidate targets and pathways for the targeted treatment of leukemia stem cells of chronic myelogenous leukemia using bioinformatics analysis

Liu

Zhuang

et al. 2019

Molec Gen & Gen Med

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Background Chronic myelogenous leukemia (CML) is a myeloproliferative neoplasm that arises from the acquisition of constitutively active BCR‐ABL tyrosine kinase in hematopoietic stem cells. The persistence of bone marrow leukemia stem cells (LSCs) is the main cause of TKI resistance and CML relapse. Therefore, finding a key target or pathway to selectively target LSCs is of great significance for the thorough treatment of CML. Methods In this study, we aimed to identify key microRNAs, microRNA targets and pathways for the treatment of CML LSCs by integrating analyses of three microarray data profiles. We identified 51 differentially expressed microRNAs through integrated analysis of GSE90773 and performed functional gene predictions for microRNAs. Then, GSE11889 and GSE11675 were integrated to obtain differentially expressed genes (DEGs), and the overlapping DEGs were used as models to identify predictive functional genes. Finally, we identified 116 predictive functional genes. Clustering and significant enrichment analysis of 116 genes was based on function and signaling pathways. Subsequently, a protein interaction network was constructed, and module analysis and topology analysis were performed on the network. Results A total of 11 key candidate targets and 33 corresponding microRNAs were identified. The key pathways were mainly concentrated on the PI3K/AKT, Ras, JAK/STAT, FoxO and Notch signaling pathways. We also found that LSCs negatively regulated endogenous and exogenous apoptotic pathways to escape from apoptosis. Conclusion We identified key candidate targets and pathways for CML LSCs through bioinformatics methods, which improves our understanding of the molecular mechanisms of CML LSCs. These candidate genes and pathways may be therapeutic targets for CML LSCs.

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MiR-122-5p inhibits cell migration and invasion in gastric cancer by down-regulating DUSP4

Abstract: MiR-122-5p restrained migration and invasion abilities of GC cells by repressing DUSP4.

Cited by 77 publications

References 34 publications

MiR‐122 inhibits epithelial mesenchymal transition by regulating P4HA1 in ovarian cancer cells

MiR‐122 inhibits epithelial mesenchymal transition by regulating P4HA1 in ovarian cancer cells

Inhibition of apoptosis by miR‑122‑5p in α‑fetoprotein‑producing gastric cancer

Identification of key candidate targets and pathways for the targeted treatment of leukemia stem cells of chronic myelogenous leukemia using bioinformatics analysis

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