Together, our findings delineate the stemness-inhibitory mechanism of miR-203 in human CRC cells and suggest that this miR is a potential therapeutic agent for colorectal cancer.
As miR‑203a‑3p was determined to target THBS2 to inhibit CRC progression and metastasis; thus, miR‑203a‑3p may be considered as a potential novel approach to treating CRC.
We evaluated psoas muscle mass index (PMI) and intramuscular adipose tissue content (IMAC) using pre-operative computed tomography imaging in 183 colorectal cancer (CRC) patients. miR-203 expression levels in CRC tissues and pre-operative serum were evaluated using quantitative polymerase chain reaction.
In summary, this study highlights an onco-miRNA role for miR-203a-3p by regulating PDE4D in CRC and suggests that miR-203a-3p may be a novel molecular therapeutic target for CRC.
These results proposed a new molecular mechanism of MALAT-miR203-DCP1A axis which is involved with the development and contributes to the malignancy of colorectal cancers.
Our results reveal the cancer-promoting effect of FBXL19-AS1, acting as a molecular sponge in negatively modulating miR-203, which might provide a new insight for understanding of CRC development.
Serum miR-203 levels were significantly upregulated in a stage-dependent manner, and high miR-203 expression was associated with poor survival in patients with CRC in both patient cohorts.
Comprehensive analyses showed that plasma miR-96 distinguished stage I-IV CRC from healthy controls with an area under curve (AUC) of 0.740; miR-203 separated stage III-IV CRC patients from stage I-II with an AUC of 0.757; and miR-141 differentiated stage IV CRC from stage I-III patients with an AUC of 0.851.
Taken together, our results provide new evidences that ZNF217 has an oncogenic role in CRC and is regulated by miR-203, and open up the possibility of ZNF217- and miR-203-targeted therapy for CRC.