MAL2 promotes proliferation, migration, and invasion through regulating epithelial-mesenchymal transition in breast cancer cell lines

Bhandari, Adheesh; Shen, Yanyan; Sindan, Namita; Xia, Erjie; Gautam, Bishnu Prasad; Lv, Shixu; Zhang, Xiaohua

doi:10.1016/j.bbrc.2018.08.187

Cited by 37 publications

(35 citation statements)

References 21 publications

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“…The downregulation of MAL2 inhibited the proliferation, migration, and invasion abilities of breast cancer cell lines. 27 Additionally, lncRNA RP11-…”

Section: Discussionmentioning

confidence: 99%

“…Recent findings have improved the understanding of the role of MAL2 in a variety of cancers, including oral squamous cell carcinoma and breast cancer. 27 , 41 Evidence in the literature showed that MAL2 was overexpressed in breast cancer cell lines. The downregulation of MAL2 inhibited the proliferation, migration, and invasion abilities of breast cancer cell lines.…”

Section: Discussionmentioning

confidence: 99%

“…The downregulation of MAL2 inhibited the proliferation, migration, and invasion abilities of breast cancer cell lines. 27 Additionally, lncRNA RP11‐284F21.9 facilitated oral squamous cell carcinoma development via the miR‐383‐5p/MAL2 axis. The knockdown of RP11‐284F21.9 could reduce the expression of MAL2 and suppress the proliferation, migration, and invasion levels of oral squamous cell carcinoma cell lines.…”

Section: Discussionmentioning

confidence: 99%

“… 25 , 26 Various pieces of evidence demonstrated the involvement of MAL2 in accelerating cell growth, migration and invasion in many cancer types, such as breast cancer, papillary thyroid cancer, and hepatocellular carcinoma. 27–29 Two studies reported the enrichment of MAL2 expression in CHOL tissues and cell lines. 30 , 31 However, the tumorigenic role of the ST8SIA6-AS1/miR-145-5p/MAL2 axis in CHOL needs to be further explored.…”

Section: Introductionmentioning

confidence: 99%

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LncRNA ST8SIA6-AS1 Promotes Cholangiocarcinoma Progression by Suppressing the miR-145-5p/MAL2 Axis

Yan

Wei

et al. 2021

OTT

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Background:The tumor-promoting roles of ST8SIA6-AS1 and miR-145-5p have been found in several cancers, but their function in cholangiocarcinoma (CHOL) remains speculative. The purpose of this study was to examine the regulatory functions of the ST8SIA6-AS1/MAL2/miR-145-5p pathway in CHOL progression. Methods: RT-qPCR assay was used to detect ST8SIA6-AS1 expression in CHOL tissues and cell lines. Cell migration, apoptosis, invasion, and proliferation abilities were assessed by RIP, RNA pull-down, and luciferase assays. CCK-8, BrdU, transwell, and FITC assays to investigate the regulatory functions of ST8SIA6-AS1, miR-145-5p, and MAL2 function in CHOL cells. Results: Findings revealed the enrichment of ST8SIA6-AS1 in CHOL tissues and cell lines. It was also found that ST8SIA6-AS1 facilitated cell growth and migration, but it reduced the apoptosis level of the CHOL cells. The results of experiments showed that ST8SIA6-AS1 sponged miR-145-5p, thereby allowing MAL2 to exert its biological function on CHOL cells. Conclusion:This research suggested that the ST8SIA6-AS1/miR-145-5p/MAL2 axis could enhance CHOL progression, which might be useful to improve the clinical outcomes of CHOL patients.

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“…The downregulation of MAL2 inhibited the proliferation, migration, and invasion abilities of breast cancer cell lines. 27 Additionally, lncRNA RP11-…”

Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

See 2 more Smart Citations

LncRNA ST8SIA6-AS1 Promotes Cholangiocarcinoma Progression by Suppressing the miR-145-5p/MAL2 Axis

Yan

Wei

et al. 2021

OTT

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“…MAP4 was involved in invasion of bladder cancer cells [210], but this gene was identified first time in GBM and may be responsible for invasion of GBM cells. Enriched genes such as RAB6B [211] and MAL2 [212] were linked with proliferation of different cancer cells types, but these genes were identified first time in GBM and may be liable for proliferation of GBM cells. Methylation inactivation of tumor suppressor DMTN (dematin actin binding protein) was associated with progression of colorectal cancer [213], but loss of this gene was identified first time in GBM and may be involved in advancement of GBM.…”

Section: Discussionmentioning

confidence: 99%

Identification of Key Genes and Signaling Pathways Associated with the Progression of Glioblastoma multiform

Vastrad¹,

Vastrad²,

Kotturshetti

2020

Preprint

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Genomic features have been gradually regarded as part of the basics to the clinical diagnosis, prognosis and treatment for glioblastoma multform (GBM). However, the molecular modifications taking place during the advancement of GBM remain unclear. Therefore, recognition of potential important genes and pathways in the gastric cancer progression is important to clinical practices. In the present study, gene expression dataset (GSE116520) of GBM were selected from the Gene Expression Omnibus (GEO) database and were further used to identify differentially expressed genes (DEGs). Then, pathway and Gene Ontology (GO) enrichment analyses were conducted, and a protein-protein interaction (PPI) network was constructed to explore the potential mechanism of GBM carcinogenesis. Significant modules were discovered using the PEWCC1 plugin for Cytoscape. In addition, a target gene - miRNA regulatory network and target gene - TF regulatory network in GBM were constructed using common deregulated miRNAs, TFs and DEGs. Finally, we carried on validation of hub genes by UALCAN, cBioporta, human protein atlas, ROC (Receiver operating characteristic) curve analysis, RT-PCR and immune infiltration analysis. The results indicated that a total of 947 differential expressed genes (DEGs) (477 up regulated and 470 down regulated) was identified in microarray profiles. Pathway enrichment analysis revealed that DEGs (up and down regulated) were mainly associated in reactive oxygen species degradation, ribosome, homocarnosine biosynthesis and GABAergic synapse, whereas GO enrichment analyses revealed that DEGs (up and down regulated) were mainly associated in macromolecule catabolic process, cytosolic part, synaptic signaling and synapse part as the main pathways associated in these processes. Finally, we filtered out hub genes, including MYC, ARRB1, RPL7A, SNAP25, SOD2, SVOP, ABCC3 and ABCA2, from the all networks. Validation of hub genes suggested the robustness of the above results. In conclusion, these results provided novel and reliable biomarkers for GBM, which will be useful for further clinical applications in GBM diagnosis, prognosis and targeted therapy.

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FTO modifies the m6A level of MALAT and promotes bladder cancer progression

Chen

et al. 2021

Clinical & Translational Med

104

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Background Nearly a half million people around the world are diagnosed with bladder cancer each year, and an incomplete understanding of its pathogenicity and lack of efficient biomarkers having been discovered lead to poor clinical management of bladder cancer. Fat mass and obesity‐associated protein (FTO) is a critical player in carcinogenesis. We, here, explored the role of FTO and unraveled the mechanism of its function in bladder cancer. Methods Identification of the correlation of FTO with bladder cancer was based on both bioinformatics and clinical analysis of tissue samples collected from a cohort of patients at a hospital and microarray data. Gain‐of‐function and loss‐of‐function assays were conducted in vivo and in vitro to assess the effect of FTO on bladder carcinoma tumor growth and its impact on the bladder carcinoma cell viability. Moreover, the interactions of intermediate products were also investigated to elucidate the mechanisms of FTO function. Results Bladder tumor tissues had increased FTO expression which correlated with clinical bladder cancer prognosis and outcomes. Both in vivo and in vitro, it played the function of an oncogene in stimulating the cell viability and tumorigenicity of bladder cancer. Furthermore, FTO catalyzed metastasis‐associated lung adenocarcinoma transcript 1 (MALAT1) demethylation, regulated microRNA miR‐384 and mal T cell differentiation protein 2 (MAL2) expression, and modulated the interactions among these processes. Conclusions The interplay of these four clinically relevant factors contributes to the oncogenesis of bladder cancer. FTO facilitates the tumorigenesis of bladder cancer through regulating the MALAT/miR‐384/MAL2 axis in m6A RNA modification manner, which ensures the potential of FTO for serving as a diagnostic or prognostic biomarker in bladder cancer.

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MAL2 promotes proliferation, migration, and invasion through regulating epithelial-mesenchymal transition in breast cancer cell lines

Cited by 37 publications

References 21 publications

LncRNA ST8SIA6-AS1 Promotes Cholangiocarcinoma Progression by Suppressing the miR-145-5p/MAL2 Axis

LncRNA ST8SIA6-AS1 Promotes Cholangiocarcinoma Progression by Suppressing the miR-145-5p/MAL2 Axis

Identification of Key Genes and Signaling Pathways Associated with the Progression of Glioblastoma multiform

FTO modifies the m6A level of MALAT and promotes bladder cancer progression

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