The role of miR-1303 in colon cancer and its possible molecular mechanism based on bioinformatics

Colon cancer is a leading global malignancy with significant health burden. As key regulators of tumorigenesis, microRNAs (miRNAs) are implicated in colon cancer progression, yet the role of miR-1303-its clinical significance and molecular mechanism-remains unclear. This study aimed to investigate the regulatory effects of miR-1303 and validate its potential as an independent prognostic indicator. miR-1303 expression was analyzed <i>via</i> qRT-PCR in 117 paired CRC tissues and adjacent normal tissues. Clinical relevance was evaluated <i>via</i> Kaplan-Meier survival curves and Cox proportional hazards modeling. Functional assays (CCK-8, Transwell migration/invasion, luciferase reporter) were performed in SW480 and HCT116 cells. Target genes were predicted using miRDB and TargetScan. Rescue experiments confirmed miR-1303 regulates CRC progression by targeting TMEM108. miR-1303 was significantly upregulated in colon cancer tissues compared to normal tissues (<i>p</i> < 0.001) and correlated with advanced TNM stage (<i>p</i> = 0.021), lymph node metastasis (<i>p</i> = 0.005), poor differentiation (<i>p</i> = 0.031), and larger tumor size (<i>p</i> = 0.044). High miR-1303 expression predicted poorer overall survival (<i>p</i> = 0.001) and was recognized as an independent predictor of prognosis (HR = 2.096, 95% CI = 1.080-4.071). Functional studies revealed that miR-1303 inhibition suppressed colon cancer cell proliferation, migration, and invasion. Mechanistically, miR-1303 directly targeted the TMEM108, leading to its post-transcriptional repression. Upregulated miR-1303 in colon cancer served as a poor prognosis predictor. miR-1303 promotes tumor progression in colon cancer by targeting TMEM108.