BACKGROUND

Colorectal cancer (CRC) is highly heterogeneous at the genetic and molecular level and a major contributor to cancer-death worldwide. Non-structural maintenance of chromosomes (SMC) condensin I complex subunit G () is a subunit of condensin I and has been shown to be associated with the prognosis of cancers. This study investigated the functional role of in CRC and its mechanism.

METHODS

Messenger RNA (mRNA) and protein expressions of and chromobox protein homolog 3 () were determined by reverse transcription-quantitative polymerase chain reaction (RT-qPCR) and western blot. The proliferation, cycle, and apoptosis of HCT116 cells were analyzed by Cell Counting Kit-8 (CCK-8), flow cytometry, and terminal deoxynucleotidyl transferase dUTP nick-end labeling (TUNEL) assay. RT-qPCR and western blot were used to determine the transfection efficacy of short hairpin (sh)-NCAPG and sh-CBX3. Western blot was used to explore cycle-, apoptosis-, and Wnt/β-catenin signaling-related proteins, and the activity of promoter was evaluated using a luciferase report assay. The expressions of cleaved caspase9 and cleaved caspase3 were assessed by colorimetric caspase activity assay.

RESULTS

The results showed that expression was elevated in CRC cells. After transfection with sh-NCAPG, expression was reduced. It was also discovered that knockdown suppressed proliferation and the cell cycle but induced apoptosis in HCT116 cells. The Human Transcription Factor Database (HumanTFDB; http://bioinfo.life.hust.edu.cn/HumanTFDB#!/) predicted the binding sites of and promoters. Meanwhile, the Encyclopedia of RNA Interactomes (ENCORI) database (https://starbase.sysu.edu.cn/) revealed that was positively correlated with . Our results showed that was transcriptionally regulated by . Additionally, Wnt/β-catenin signaling was discovered to be activated by overexpression. Further experiments showed that transcriptionally regulated by activated Wnt/β-catenin signaling to regulate the proliferation, cell cycle, and apoptosis of HCT116 cells.

CONCLUSIONS

Collectively, the results of our study indicated that was transcriptionally regulated by and activated the Wnt/β-catenin signaling pathway to facilitate the progression of CRC.