Colorectal cancer (CRC) is a common digestive tract malignancy, which is characterized by high mortality, morbidity, and poor prognosis. Replication factor C subunit 2 (RFC2), one RFC family member, was reported to be related to various malignancies and plays an important role in proliferation, invasion, and metastasis. Nonetheless, the RFC2 biological role within CRC is still unknown. RFC2 expression profiles in CRC tissues were collected based on The Cancer Genome Atlas database, whereas miR‐744 and RFC2 expression levels were detected in human CRC tissues. miR‐744 and RFC2 effects on the proliferation of CRC were assessed both in vivo and in vitro. RFC2 was recognized to be a direct miR‐744 target through luciferase reporter assay. RFC2 upregulation was observed within CRC tissues, and a high RFC2 level showed a correlation with poor clinicopathological symptoms. RFC2 knockdown inhibited CRC cell proliferation through promoting cell cycle arrest at the G1 phase, which was achieved by cyclin E2 (CCNE2) downregulation in vivo and in vitro. miR‐744 was identified to be the tumor suppressor microRNA, which targeted RFC2 directly for inhibiting the proliferation of CRC cells both in vivo and in vitro. miR‐744 downregulation was detected within CRC tissue, and messenger RNA expression showed a negative correlation with RFC2 expression within CRC tissues. Our study demonstrates that the miR‐744/RFC2/CCNE2 axis potentially provides a candidate for a treatment strategy for CRC.

The complex in which scribble planar cell polarity protein (SCRIB) is located is one of the three main polar protein complexes that play an important role in maintaining epithelial polarity and affecting tumour growth. However, the role of SCRIB in colorectal cancer (CRC) remains largely unknown. This study used date from The Cancer Genome Atlas (TCGA) and clinical samples to determine the expression of SCRIB in CRC and explored its mechanism through bioinformatics analysis and in vivo and in vitro experiments. In this study, SCRIB was found to be highly expressed in CRC patients, and it was often associated with malignant characteristics, such as proliferation, apoptosis, and epithelial-mesenchymal transition (EMT). Furthermore, we found that SCRIB may interact with the Hippo signalling pathway and affect the phosphorylation of YAP and its distribution inside and outside of the nucleus. We concluded that increased expression of SCRIB is likely to inhibit the Hippo signalling pathway by promoting YAP phosphorylation. This role of SCRIB in the progression of CRC provides an important information for the treatment of CRC.

This study first confirmed the key role of miR-361-3p in hypoxic EVs in promoting proliferation and inhibiting apoptosis of CRC cells. • miR-361-3p promotes CRC progression by targeting the TRAF3-mediated noncanonical NF-kB pathway. • HIF-1α is the key factor for hypoxic exosomal miR-361-3p elevation in CRC cells.