The functions of long non-coding RNA (lncRNA)-MALAT-1 in the pathogenesis of renal cell carcinoma

Abstract

Renal cell carcinoma (RCC), a prevalent form of renal malignancy, is distinguished by its proclivity for robust tumor proliferation and metastatic dissemination. Long non-coding RNAs (lncRNAs) have emerged as pivotal modulators of gene expression, exerting substantial influence over diverse biological processes, encompassing the intricate landscape of cancer development. Metastasis-associated lung adenocarcinoma transcript 1 (MALAT-1), an exemplar among lncRNAs, has been discovered to assume functional responsibilities within the context of RCC. The conspicuous expression of MALAT-1 in RCC cells has been closely linked to the advancement of tumors and an unfavorable prognosis. Experimental evidence has demonstrated the pronounced ability of MALAT-1 to stimulate RCC cell proliferation, migration, and invasion, thereby underscoring its active participation in facilitating the metastatic cascade. Furthermore, MALAT-1 has been implicated in orchestrating angiogenesis, an indispensable process for tumor expansion and metastatic dissemination, through its regulatory influence on pro-angiogenic factor expression. MALAT-1 has also been linked to the evasion of immune surveillance in RCC, as it can regulate the expression of immune checkpoint molecules and modulate the tumor microenvironment. Hence, the potential utility of MALAT-1 as a diagnostic and prognostic biomarker in RCC emerges, warranting further investigation and validation of its clinical significance. This comprehensive review provides an overview of the diverse functional roles exhibited by MALAT-1 in RCC.

MALAT-1 Is a Key Regulator of Epithelial–Mesenchymal Transition in Cancer: A Potential Therapeutic Target for Metastasis

“…MALAT-1 induces cancer proliferation, invasion, migration, and metastasis to distant sites. Recently, several studies highlighted the immunomodulatory role of MALAT-1 and how it can enable cancer cells to escape immune surveillance by exerting an immunosuppressive effect and regulating the expression of several molecules associated with the tumor microenvironment [ 9 , 10 ]. In the triple-negative breast cancer (TNBC) cell model, MALAT-1 knockdown results in a marked induction in MHC class I chain-related proteins A/B expression and the repression of the checkpoint molecules PD-L1 and B7-H4 [ 11 ].…”