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Colon cancer has a high mortality rate, thus there is an urgent need to develop novel therapeutic options for clinical management of the disease. Studies have revealed that chaperonin containing TCP1 subunit 6A (CCT6A) promoted the development of multiple types of cancer, and dataset analysis revealed that homeobox B2 (HOXB2) has the potential to modulate the expression of CCT6A. However, whether HOXB2 affects the proliferation, migration and invasion of colon cancer cells remains to be determined. A CCT6A knockdown colon cancer cell line was established and colony formation, wound healing and Transwell invasion assays were performed to assess proliferation, migration and invasion of the altered colon cancer cells. Subsequently, luciferase reporter gene assays and chromatin immunoprecipitation assays were performed to detect the relationship between HOXB2 and CCT6A. A HOXB2 overexpression colon cancer cell line was established and the proliferation, migration and invasion of these cells was determined using the same methods. Knockdown of CCT6A reduced the proliferation, migration and invasion of colon cancer cells. HOXB2 enhanced the expression of CCT6A in colon cancer cells by binding to the promoter of CCT6A. Overexpression of HOXB2 abolished the inhibitory effect of CCT6A knockdown on the proliferation, migration and invasion of colon cancer cells. HOXB2 increased the proliferation and invasiveness of colon cancer cells by increasing the expression of CCT6A.

Overcoming resistance to chemotherapy is an arduous challenge in the treatment of colorectal cancer (CRC), particularly since the underlying molecular mechanisms remain obscure. In the present study, we reported that miR‑874-3p was markedly downregulated in CRC tissues compared with that in adjacent normal colorectal epithelial tissues. Upregulation of miR-874-3p attenuated the chemoresistance of CRC cells to 5-fluorouracil (5-FU) in vitro and in vivo. Conversely, inhibition of miR-874-3p yielded an opposite effect. Furthermore, our results demonstrated that miR-874-3p directly inhibited the expression of transcriptional co-activators YAP and TAZ of the Hippo signaling pathway, resulting in the inactivation of the TEAD transcription. Thus, our findings clarify a novel mechanism by which miR-874-3p restores chemotherapeutic sensitivity of CRC to 5-FU, indicating that offering miR-874-3p mimics in combination with 5-FU may serve as a new therapeutic strategy to circumvent the chemoresistance in CRC.