![]() This in turn triggers DNA damage and ultimately apoptosis to achieve therapeutic effects. Oxaliplatin, a third-generation chemotherapeutic agent, works by reacting with DNA in the S-phase to form intra- and inter-strand cross-linked hydrated derivatives. Currently, oxaliplatin-based chemotherapy is highly effective in locally advanced CRC or metastatic CRC. CRC is a common gastrointestinal malignancy with a rising incidence and mortality rate. ![]() The incidence and mortality rate of colorectal cancer (CRC) are increasing each year. In conclusion, this study identified AC092894.1 as a suppressor of CRC chemoresistance and revealed the idea that targeting the AC092894.1/USP3/AR/RASGRP3 signaling axis is a novel option for the treatment of oxaliplatin resistance. Finally, sustained activation of the MAPK signaling pathway induced apoptosis in CRC cells. Studies on the mechanism suggested that AC092894.1 served as a scaffold molecule that mediated the de-ubiquitination of AR through USP3, thereby increasing the transcription of RASGRP3. In vivo and in vitro experiments revealed that AC092894.1 functions to reverse chemoresistance. ![]() ![]() ResultsĪC092894.1 representation has been demonstrated to be drastically downregulated throughout oxaliplatin-induced drug-resistant CRC cells. Finally, the potential mechanism of AC092894.1 was explored by RNA pull-down, RIP, and Co-IP experiments. lncRNA effects on oxaliplatin chemoresistance were then verified by gain- and loss-of-function experiments. The lncRNAs associated with oxaliplatin resistance were screened by microarray. Recently, long non-coding RNAs (lncRNAs) have emerged as novel molecules for the treatment of chemoresistance, but the specific molecular mechanisms mediated by them are poorly understood. Oxaliplatin resistance is a complex process and has been one of the most disadvantageous factors and indeed a confrontation in the procedure of colorectal cancer.
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