Integrin subunit alpha V promotes growth, migration, and invasion of gastric cancer cells

Wang, Huashe; Chen, Honglei; Jiang, Zhipeng; Lin, Yujun; Wang, Xinyou; Xiang, Jun; Peng, Junsheng

doi:10.1016/j.prp.2019.152531

Cited by 46 publications

(42 citation statements)

References 24 publications

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“…Through iTRAQ quantitative proteomics, we found that the expression of ITGAV protein in CCA samples was stronger than that in nontumour samples, which was consistent with the results at the mRNA level. This finding is also consistent with the expression of ITGAV in gastric cancer, but overexpression of ITGAV has been found to be associated with a poor prognosis in gastric cancer patients [29]. Kang et al reported that lncRNA AY can promote hepatocellular carcinoma metastasis by inducing transcription of ITGAV [32].…”

Section: Discussionsupporting

confidence: 74%

“…Integrin subunit alpha V (ITGAV), a member of the integrin family, has been found to be associated with cell differentiation and metastasis and can serve as a prognostic biomarker for a variety of cancers [29][30][31]. In our study, we found that ITGAV mRNA expression was significantly upregulated in CCA and that upregulated expression was associated with better prognosis in CCA patients through bioinformatics analysis.…”

Section: Discussionmentioning

confidence: 60%

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Bioinformatics combined with quantitative proteomics analyses and identification of potential biomarkers in cholangiocarcinoma

Gao

et al. 2020

Cancer Cell Int

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Background: Cholangiocarcinoma (CCA) is an invasive malignancy arising from biliary epithelial cells; it is the most common primary tumour of the bile tract and has a poor prognosis. The aim of this study was to screen prognostic biomarkers for CCA by integrated multiomics analysis. Methods: The GSE32225 dataset was derived from the Gene Expression Omnibus (GEO) database and comprehensively analysed by using R software and The Cancer Genome Atlas (TCGA) database to obtain the differentially expressed RNAs (DERNAs) associated with CCA prognosis. Quantitative isobaric tags for relative and absolute quantification (iTRAQ) proteomics was used to screen differentially expressed proteins (DEPs) between CCA and nontumour tissues. Through integrated analysis of DERNA and DEP data, we obtained candidate proteins APOF, ITGAV and CASK, and immunohistochemistry was used to detect the expression of these proteins in CCA. The relationship between CASK expression and CCA prognosis was further analysed. Results: Through bioinformatics analysis, 875 DERNAs were identified, of which 10 were associated with the prognosis of the CCA patients. A total of 487 DEPs were obtained by using the iTRAQ technique. Comprehensive analysis of multiomics data showed that CASK, ITGAV and APOF expression at both the mRNA and protein levels were different in CCA compared with nontumour tissues. CASK was found to be expressed in the cytoplasm and nucleus of CCA cells in 38 (45%) of 84 patients with CCA. Our results suggested that patients with positive CASK expression had significantly better overall survival (OS) and recurrence-free survival (RFS) than those with negative CASK expression. Univariate and multivariate analyses demonstrated that negative expression of CASK was a significantly independent risk factor for OS and RFS in CCA patients. Conclusions: CASK may be a tumour suppressor; its low expression is an independent risk factor for a poor prognosis in CCA patients, and so it could be used as a clinically valuable prognostic marker.

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Section: Discussionsupporting

confidence: 74%

Section: Discussionmentioning

confidence: 60%

Bioinformatics combined with quantitative proteomics analyses and identification of potential biomarkers in cholangiocarcinoma

Gao

et al. 2020

Cancer Cell Int

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“…In ovarian cancer, increased ITGB1 enhanced metastasis by mediating ECM remodeling (45). In GC, ITGAV overexpression was responsible for cell migration and invasion and was associated with poor prognosis (46). Recently, extensive studies have suggested that metastasis and drug resistance are intrinsically linked (47).…”

Section: Discussionmentioning

confidence: 99%

Regulation of Integrin Subunit Alpha 2 by miR-135b-5p Modulates Chemoresistance in Gastric Cancer

et al. 2020

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Chemotherapy has substantially improved gastric cancer (GC) patient outcomes in the past decades. However, the development of chemotherapy resistance has become the major cause of treatment failure. Although numerous molecules have been implicated in GC chemoresistance, its pathological mechanisms are still unclear. Here, we found that integrin subunit alpha 2 (ITGA2) is upregulated in chemoresistant GC cells and that increased ITGA2 levels correlated with the poor prognosis of GC patients who received chemotherapy. ITGA2 overexpression led to elevated chemotherapy resistance and drug-induced apoptosis inhibition in GC cells. ITGA2 knockdown resulted in restored chemosensitivity and increased apoptosis in chemoresistant GC cells both in vitro and in vivo. NanoString analysis revealed a unique signature of deregulated pathway expression in GC cells after ITGA2 silencing. The MAPK/ERK pathway and epithelial-mesenchymal transition (EMT) were found to be downregulated after ITGA2 knockdown. miR-135b-5p was identified as a direct upstream regulator of ITGA2. miR-135b-5p overexpression reduced chemoresistance and induced apoptosis in GC cells and attenuated ITGA2-induced chemoresistance and antiapoptotic effects by inhibiting MAPK signaling and EMT. In conclusion, this study underscored the role and mechanism of ITGA2 in GC and suggested the novel miR-135b-5p/ITGA2 axis as an epigenetic cause of chemoresistance with diagnostic and therapeutic implications.

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“…Numerous evidence indicates that up-regulation of CD51 is significantly associated with cancer progression and poor prognosis in multiple types of cancers, such as gastric cancer (Wang et al, 2019), osteosarcoma (Pei et al, 2019), colorectal cancer (Flum et al, 2018), and nasopharyngeal carcinoma (Ding et al, 2017). The expressions and functions of CD51 have been shown to be dysregulated in prostate cancer.…”

Section: Discussionmentioning

confidence: 99%

“…CD51, also known as integrin subunit alpha V (ITGAV), is a member of the integrin alpha chain family (Conroy et al, 2016). Several evidences have indicated that the up-regulation of CD51 is significantly associated with cancer progression and poor prognosis in multiple types of cancers, such as gastric cancer (Wang et al, 2019), colorectal cancer (Flum et al, 2018), laryngeal carcinoma (Lu et al, 2009), and hepatocellular carcinoma (Kang et al, 2019). Mechanically, it was confirmed that CD51 could inhibit the expression of E-cadherin and promote epithelial-tomesenchymal transition (EMT) by interacting with transforming growth factor-beta (Feldkoren et al, 2017).…”

Section: Introductionmentioning

confidence: 99%

Long Non-coding RNA SNHG17 Promotes Cell Proliferation and Invasion in Castration-Resistant Prostate Cancer by Targeting the miR-144/CD51 Axis

et al. 2020

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Previously, we found that the expression of long non-coding RNA (lncRNA) small nucleolar RNA host gene 17 (SNHG17) was up-regulated in castration-resistant prostate cancer (CRPC) cells compared to that in hormone sensitive prostate cancer (HSPC) cells. Moreover, we found that CD51 was up-regulated in prostate cancer cells and promoted the carcinogenesis and progression of prostate cancer. However, the regulatory mechanism of SNHG17 and CD51 in the development of CRPC remains unclear. In the current study, we aimed to elucidate the expressions, functions, and underlying mechanism of SNHG17 and CD51 in CRPC. Our results further confirmed that both SNHG17 and CD51 were up-regulated in CRPC tissues and cells. In addition, we found that SNHG17 expression was positively correlated with CD51 expression in prostate cancer. Mechanically, SNHG17 functioned as a competing endogenous RNA (ceRNA) to up-regulate CD51 expression through competitively sponging microRNA-144 (miR-144), and CD51 was identified as a direct downstream target of miR-144 in CRPC. Functionally, down-regulation of SNHG17 or up-regulation of miR-144 inhibited the proliferation, migration, and invasion of CRPC cells, whereas up-regulation of SNHG17 and down-regulation of miR-144 promoted the proliferation, migration and invasion of CRPC cells in vitro and in vivo. Using gain and loss-of function assay and rescue assay, we showed that miR-144 inhibited cell proliferation, migration and invasion by directly inhibiting CD51 expression, and SNHG17 promoted cell proliferation, migration and invasion by directly enhancing CD51 expression in CRPC cells. Taken together, our study reveals the role of the SNHG17/miR-144/CD51 axis in accelerating CRPC cell proliferation and invasion, and suggests that SNHG17 may serve as a novel therapeutic target for CRPC.

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Integrin subunit alpha V promotes growth, migration, and invasion of gastric cancer cells

Cited by 46 publications

References 24 publications

Bioinformatics combined with quantitative proteomics analyses and identification of potential biomarkers in cholangiocarcinoma

Bioinformatics combined with quantitative proteomics analyses and identification of potential biomarkers in cholangiocarcinoma

Regulation of Integrin Subunit Alpha 2 by miR-135b-5p Modulates Chemoresistance in Gastric Cancer

Long Non-coding RNA SNHG17 Promotes Cell Proliferation and Invasion in Castration-Resistant Prostate Cancer by Targeting the miR-144/CD51 Axis

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