Beyond the genome: MALAT1's role in advancing urologic cancer care

Urologic cancers (UCs), which include bladder, kidney, and prostate tumors, account for almost a quarter of all malignancies. Long non-coding RNAs (lncRNAs) are tissue-specific RNAs that influence cell growth, death, and division. LncRNAs are dysregulated in UCs, and their abnormal expression may al...

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Bibliographic Details
Published in:Pathology, research and practice research and practice, 2024-04, Vol.256, p.155226-155226, Article 155226
Main Authors: Imran, Mohd, Abida, Eltaib, Lina, Siddique, Muhammad Irfan, Kamal, Mehnaz, Asdaq, Syed Mohammed Basheeruddin, Singla, Neelam, Al-Hajeili, Marwan, Alhakami, Fatemah Abdulaziz, AlQarni, Ahmed Farhan, Abdulkhaliq, Altaf A., Rabaan, Ali A.
Format: Article
Language:English
Subjects:
Cell cycle
MALAT1
Pathology
Treatment
Urologic cancer
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Summary:Urologic cancers (UCs), which include bladder, kidney, and prostate tumors, account for almost a quarter of all malignancies. Long non-coding RNAs (lncRNAs) are tissue-specific RNAs that influence cell growth, death, and division. LncRNAs are dysregulated in UCs, and their abnormal expression may allow them to be used in cancer detection, outlook, and therapy. With the identification of several novel lncRNAs and significant exploration of their functions in various illnesses, particularly cancer, the study of lncRNAs has evolved into a new obsession. MALAT1 is a flexible tumor regulator implicated in an array of biological activities and disorders, resulting in an important research issue. MALAT1 appears as a hotspot, having been linked to the dysregulation of cell communication, and is intimately linked to cancer genesis, advancement, and response to treatment. MALAT1 additionally operates as a competitive endogenous RNA, binding to microRNAs and resuming downstream mRNA transcription and operation. This regulatory system influences cell growth, apoptosis, motility, penetration, and cell cycle pausing. MALAT1's evaluation and prognosis significance are highlighted, with a thorough review of its manifestation levels in several UC situations and its association with clinicopathological markers. The investigation highlights MALAT1's adaptability as a possible treatment target, providing fresh ways for therapy in UCs as we integrate existing information The article not only gathers current knowledge on MALAT1's activities but also lays the groundwork for revolutionary advances in the treatment of UCs.
ISSN:0344-0338
1618-0631
DOI:10.1016/j.prp.2024.155226