Long non-coding RNA activated in renal cell carcinoma with sunitinib resistance (lncARSR)

Long non-coding RNA activated in renal cell carcinoma with sunitinib resistance (lncARSR) is a regulatory RNA (>200 nucleotides) that does not code for protein but plays a central role in tumor biology and drug resistance. lncARSR is highly expressed in resistant RCC and other tumors such as HCC and NSCLC, where it promotes cell survival, proliferation, migration, and resistance to therapies such as sunitinib and adriamycin. Mechanistically, lncARSR functions as a molecular sponge for specific microRNAs such as miR-34 and miR-449, leading to increased expression of oncogenic receptors (AXL, c-MET) and activation of downstream signaling pathways (STAT3, AKT, ERK). Plasma and tissue levels of lncARSR have been associated with poor prognosis and are explored as predictive biomarkers for therapy response. The targeting of lncARSR is considered promising for overcoming drug resistance in several cancers, though clinical translation is still in early exploratory stages[2][6][7][10].

Other names

lnc-TALClncRNA regulator of Akt signaling associated with HCC and RCCtemozolomide-associated lncRNA in glioblastoma recurrence

Acts as a competing endogenous RNA (“sponges” miR-34/miR-449), upregulating AXL and c-MET, thereby activating STAT3, AKT, and ERK pathways and conferring resistance to sunitinib in RCC. Promotes resistance to other drugs such as adriamycin in other cancer contexts by interfering with miRNA-mediated regulation of pro-oncogenic signaling.