miR-450b-3p inhibited the proliferation of gastric cancer via regulating KLF7

Yao, Juan; Zhang, Hao; Liu, Cheng; Chen, Shuangshuang; Ran, Qian; Zhao, Kun

doi:10.1186/s12935-020-1133-2

Cited by 22 publications

(15 citation statements)

References 23 publications

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“…Furthermore, according to previous studies, patients with GC regularly exhibit partial metastasis at diagnosis or during chemotherapy ( 4 , 5 ). Despite advances in GC diagnostic techniques, surgery and neoadjuvant chemoradiotherapy, the 5-year survival rate remains poor in China, particularly at advanced stages ( 6 , 7 ). Owing to the complexity of the pathogenesis of GC, its underlying molecular mechanisms remain unclear.…”

Section: Introductionmentioning

confidence: 99%

CBX2 depletion inhibits the proliferation, invasion and migration of gastric cancer cells by inactivating the YAP/β-catenin pathway

Zeng

Yang

et al. 2020

Mol Med Rep

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Gastric cancer (GC) is the most common and fast-growing malignancy of the digestive system, which has a high mortality. Chromobox homolog 2 (CBX2) has been reported to be highly expressed in cancer tissues compared with adjacent normal tissues. It has also been established that CBX2 is upregulated in GC cell lines by searching the Cancer Cell Line Encyclopedia. The aim of the present study was to investigate the biomolecular role and underlying mechanism of CBX2 in the proliferation, invasion and migration of GC cells. Short hairpin RNA-CBX2 and yes-associated protein (YAP) overexpression plasmids were constructed to regulate CBX2 and YAP expression, respectively. Additionally, the expression of certain mRNAs and proteins involved in the YAP/β-catenin pathway and those associated with cell invasion were assessed by western blotting and reverse transcription-quantitative PCR, respectively. The cellular behaviors of MFC cells were analyzed using Cell Counting Kit-8, colony formation wound-healing and Transwell assays. The results of the present study revealed that increased CBX2 expression was observed in GC cell lines compared with normal gastric cells. In addition, CBX2 knockdown inhibited the nuclear cytoplasm translocation of YAP, inducing its phosphorylation, and suppressing the activation of the β-catenin signaling pathway. The results also demonstrated that CBX2 depletion inhibited the proliferation, migration and invasion of GC cells by inactivating the YAP/β-catenin pathway. It was determined that CBX2 promoted the proliferation, invasion and migration of GC cells by activating the YAP/β-catenin pathway, suggesting that CBX2 is involved in the pathogenesis of GC and may represent a novel target for the clinical treatment of GC.

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Section: Introductionmentioning

confidence: 99%

CBX2 depletion inhibits the proliferation, invasion and migration of gastric cancer cells by inactivating the YAP/β-catenin pathway

Zeng

Yang

et al. 2020

Mol Med Rep

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“…Nowadays, increasing studies have proved that a series of miRNAs are involved in progression of multiple styles of tumors [7][8][9][10][11][12][13]. For instance, miR-662 [6], miR-532-5p [14], miR-199a [15], miR-940 [24], miR-200b [17], miR-34a [18], miR-130b [19], and miR-148a [20] all play an essential role in gliomas. Herein, we investigated the role of miR-136-3p and its target gene KLF7 in glioma development.…”

Section: Discussionmentioning

confidence: 99%

“…Integration of this bioinformatic analysis with the previous studies, we observed that KLF7 was a direct target of miR-136-3p in gliomas. In the previous studies, KLF3, targeted by miR-450b-3p and miR-185, often severs as an oncogene in gastric cancer [18] and non-small cell lung cancer respectively [19]. And KLF7, regulated by Linc00669/miR-193a axis, may also promote progression of non-small cell lung cancer [20].…”

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confidence: 93%

MicroRNA-136-3p inhibits glioma tumorigenesis in vitro and in vivo by targeting KLF7

Xu¹

2020

World J Surg Onc

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Background: Malignant brain tumors have been a serious threat to human health worldwide. This study aims to investigate the role of miR-136-3p in glioma development. Methods: Hematoxylin-eosin staining (H&E) staining was used to determine the pathologic alterations of glioma tissues. Quantitative real-time PCR (qRT-PCR) analysis and GEO2R analysis was performed to examine the expression of miRNAs and genes. Western blot was applied to detect the protein expression. Cell counting kit-8 (CCK-8) and colony formation were used to analyze the glioma cell growth. Trans-well assay was used to determine the cell migration. Annexin V-FITC/PI staining was conducted to determine the cell apoptosis of transfected glioma cells. The dual-luciferase reporter assay was carried out to confirm the binding sites of miR-136-3p on 3′ untranslated regions (3′ UTR) of Kruppel-like factor 7 (KLF7). Tumor-bearing experiment in nude mice was performed to comprehensively investigate the role of miR-136-3p/KLF7 axis in gliomas. Results: Firstly, the results showed that miR-136-3p was decreased in glioma tissues compared with adjacent tissues. Overexpression of miR-136-3p significantly inhibited cell growth of LN-229 and U251 by decreasing expression of Cyclin A1 and PCNA (proliferating cell nuclear antigen), and it suppressed glioma cell migration by downregulating N-cadherin and elevating E-cadherin levels, and it also promotes glioma cell apoptosis by promoting Bcl2-associated X (Bax) expression but suppressing Bcl-2 expression. Furthermore, we observed that KLF7 was a direct target of miR-136-3p, and KLF7 was negatively regulated by miR-136-3p in glioma cells. Finally, overexpression of KLF7 partly blocked miR-136-3p-induced inhibition of tumor growth in vitro and in vivo. Conclusions: Targeting miR-136-3p/KLF7 axis might be a novel manner to counter against gliomas.

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“…MicroRNAs (miRNAs), also belonging to non-coding RNAs (ncRNAs), emerge as a type of endogenous ncRNAs with 19-24 nucleotides, and can bind to the 3ʹ-UTR of target mRNA to further modulate the target gene expression. 12 In addition, miRNAs take part in regulating the malignant phenotypes of cancer cells in many different tumors including GC, such as cell proliferation, differentiation and apoptosis. [13][14][15] For example, miR-638 is down-regulated in GC, and its overexpression suppresses cell growth via inhibiting MACCI expression.…”

Section: Introductionmentioning

confidence: 99%

<p>LncRNA CTBP1-AS2 Facilitates Gastric Cancer Progression via Regulating the miR-139-3p/MMP11 Axis</p>

Yang

Gao

Liu

et al. 2020

OTT

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Background This study aimed at probing into the effect of long non-coding RNA (lncRNA) C-terminal binding protein 1 antisense RNA 2 (CTBP1-AS2) on gastric cancer (GC) cell proliferation and apoptosis, and its regulatory function on miR-139-3p and MMP11 . Methods Quantitative real-time polymerase chain reaction (qRT-PCR) was employed to examine the expressions of CTBP1-AS2, miR-139-3p and MMP11 mRNA in GC cell lines and clinical specimens. Cell counting kit-8 (CCK-8) assay, flow cytometry and EdU assay were conducted to examine the effects of CTBP1-AS2 and miR-139-3p on GC cell proliferation and apoptosis. Western blot was applied for detecting the expressions of Bax, Bcl-2 and MMP11 . A lung metastasis mouse model was used to evaluate metastasis of GC cells in vivo. Bioinformatics, dual-luciferase report assay, RIP and RNA pull-down assays were utilized to validate the targeted relationship between CTBP1-AS2 and miR-139-3p as well as the targeting relationship between miR-139-3p and MMP11 . Results CTBP1-AS2 was highly expressed in GC, and its high expression was strongly associated with increased TNM stage, increased tumor size and low degree of differentiation of the tumor tissues. Meanwhile, CTBP1-AS2 promoted GC cell proliferation, metastasis and suppressed apoptosis, while miR-139-3p could weaken these effects. In addition, CTBP1-AS2 was identified as a molecular sponge for miR-139-3p, and MMP11 was verified as a target gene of CTBP1-AS2. CTBP1-AS2 could increase the expression of MMP11 via repressing miR-139-3p. Conclusion CTBP1-AS2 promotes GC cells and inhibits apoptosis by regulating the miR-139-3p/ MMP11 molecular axis.

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miR-450b-3p inhibited the proliferation of gastric cancer via regulating KLF7

Cited by 22 publications

References 23 publications

CBX2 depletion inhibits the proliferation, invasion and migration of gastric cancer cells by inactivating the YAP/β-catenin pathway

CBX2 depletion inhibits the proliferation, invasion and migration of gastric cancer cells by inactivating the YAP/β-catenin pathway

MicroRNA-136-3p inhibits glioma tumorigenesis in vitro and in vivo by targeting KLF7

<p>LncRNA CTBP1-AS2 Facilitates Gastric Cancer Progression via Regulating the miR-139-3p/MMP11 Axis</p>

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