GAS5 lncRNA: A biomarker and therapeutic target in breast cancer.

Autor: Thangavelu L; Center for Global Health Research, Saveetha Medical College, Saveetha Institute of Medical and Technical Sciences, India., Moglad E; Department of Pharmaceutics, College of Pharmacy, Prince Sattam Bin Abdulaziz University, Al Kharj 11942, Saudi Arabia., Gupta G; Centre for Research Impact & Outcome-Chitkara College of Pharmacy, Chitkara University, Punjab, India., Menon SV; Department of Chemistry and Biochemistry, School of Sciences, JAIN (Deemed to be University), Bangalore, Karnataka, India., Gaur A; Graphic Era (Deemed to be University), Clement Town, Dehradun 248002, India; Graphic Era Hill University, Clement Town, Dehradun 248002, India., Sharma S; Chandigarh Pharmacy College, Chandigarh Group of Colleges, Jhanjheri, Mohali, Punjab 140307, India., Kaur M; Department of Sciences, Vivekananda Global University, Jaipur, Rajasthan 303012, India., Chahar M; Department of Chemistry, NIMS University, Jaipur, India., Sivaprasad GV; Department of Basic Science & Humanities, Raghu Engineering College, Visakhapatnam, India., Deorari M; Uttaranchal Institute of Pharmaceutical Sciences, Uttaranchal University, Dehradun, India. Electronic address: deoraripharma@hotmail.com.
Jazyk: angličtina
Zdroj: Pathology, research and practice [Pathol Res Pract] 2024 Aug; Vol. 260, pp. 155424. Date of Electronic Publication: 2024 Jun 20.
DOI: 10.1016/j.prp.2024.155424
Abstrakt: Breast cancer is one of the most common causes of cancer-related mortality globally, and its aggressive phenotype results in poor treatment outcomes. Growth Arrest-Specific 5 long non-coding RNA has attracted considerable attention due to its pivotal function in apoptosis regulation and tumor aggressiveness in breast cancer. Gas5 enhances apoptosis by regulating apoptotic proteins, such as caspases and BCL2 family proteins, and the sensitivity of BCCs to chemotherapeutic agents. At the same time, low levels of GAS5 increased invasion, metastasis, and overall tumor aggressiveness. GAS5 also regulates EMT markers, critical for cancer metastasis, and influences tumor cell proliferation by regulating various signaling components. As a result, GAS5 can be restored to suppress tumor development as a possible therapeutic strategy, which might present promising prospects for a patient's treatment. Its activity levels might also be a crucial indicator and diagnostic parameter for prediction. This review highlights the significant role of GAS5 in modulating apoptosis and tumor aggressiveness in breast cancer, emphasizing its potential as a therapeutic target for breast cancer treatment and management.
Competing Interests: Declaration of Competing Interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper.
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Databáze: MEDLINE