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The functions of long non-coding RNA (lncRNA)-MALAT-1 in the pathogenesis of renal cell carcinoma
O. Anbiyaee, A. Moalemnia, F. Ghaedrahmati, MK. Shooshtari, SE. Khoshnam, B. Kempisty, SA. Halili, M. Farzaneh, OB. Morenikeji
Jazyk angličtina Země Anglie, Velká Británie
Typ dokumentu časopisecké články, přehledy
NLK
BioMedCentral
od 2000-12-01
BioMedCentral Open Access
od 2000
Directory of Open Access Journals
od 2000
Free Medical Journals
od 2000
PubMed Central
od 2000
ProQuest Central
od 2009-01-01
Open Access Digital Library
od 2000-10-01
Open Access Digital Library
od 2000-01-01
Open Access Digital Library
od 2000-01-01
Medline Complete (EBSCOhost)
od 2000-10-04
Health & Medicine (ProQuest)
od 2009-01-01
ROAD: Directory of Open Access Scholarly Resources
od 2000
Springer Nature OA/Free Journals
od 2000-12-01
- MeSH
- karcinom z renálních buněk * genetika patologie MeSH
- lidé MeSH
- nádorové buněčné linie MeSH
- nádorové mikroprostředí genetika MeSH
- nádory ledvin * genetika patologie MeSH
- prognóza MeSH
- proliferace buněk genetika MeSH
- RNA dlouhá nekódující * genetika metabolismus MeSH
- Check Tag
- lidé MeSH
- Publikační typ
- časopisecké články MeSH
- přehledy MeSH
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.
Chronic Renal Failure Research Center Ahvaz Jundishapur University of Medical Sciences Ahvaz Iran
Department of Immunology School of Medicine Isfahan University of Medical Sciences Isfahan Iran
Division of Biological and Health Sciences University of Pittsburgh at Bradford Bradford PA USA
Faculty of Medicine Dezful University of Medical Sciences Dezful Iran
Physiology Graduate Faculty North Carolina State University Raleigh NC 27695 US
Citace poskytuje Crossref.org
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- $a 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.
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