No abstract

In recent years, extensive reports have been published concerning the molecular mechanism underlying the occurrence and progression of colorectal cancer. Circular RNAs (circRNAs) have been identified as important modulators in the biological processes of colorectal cancer. Microarray analysis unveiled that differential circ‐0004277 expression was identified in tissue samples of colorectal cancer. High circ‐0004277 expression was then verified in tissue samples and cell lines of colorectal cancer via qRT‐PCR. Kaplan–Meier analysis was used for identifying the association between circ‐0004277 expression and the overall survival rate of colorectal cancer patients. A relationship existed between higher circ‐0004277 expression and decreased overall survival rate of colorectal cancer patients. From a functional perspective, circ‐0004277 knockdown accelerated cell apoptosis and restrained cell proliferation of colorectal cancer. From mechanistic perspective, circ‐0004277 upregulated PTMA by sponging miR‐512‐5p. Rescue assay was used for verifying the roles of the circ‐0004277‐miR‐512‐5p‐PTMA axis. Both miR‐512‐5p and PTMA participated in circ‐0004277‐mediated colorectal cancer cell proliferation based on experiments. In summary, our study showed that circ‐0004277 promoted the proliferation of colorectal cancer cells as a miR‐512‐5p sponge to upregulate the PTMA expression.

Aim: In this study, we aim to use bioinformatics approach to identify paclitaxel-targeted modulators potentially involved in the process of reversing the trastuzumab resistance. Materials & methods: We extracted data from GSE77346 to identify potential trastuzumab resistance-related genes, used bioinformatics analysis and functional/activity network approach to find genes involved in trastuzumab resistance reversal. Results: We identified hub differentially expressed genes related to trastuzumab resistance, trastuzumab targeting and paclitaxel targeting, respectively. We then found C-Jun may be critical in trastuzumab resistance reversal.  This process may involve transcriptional activation of DUSP1 by JUN, which lead to regulation of DUSP1-related signaling pathways. Conclusion: The present study revealed paclitaxel may reverse the trastuzumab resistance by JUN, which possibly in turn regulated DUSP1 and DUSP1-related signaling pathways.