Important role and underlying mechanism of non­SMC condensin I complex subunit G in tumours (Review).

At present, the incidence of tumours is increasing on a yearly basis, and tumourigenesis is usually associated with chromosomal instability and cell cycle dysregulation. Moreover, abnormalities in the chromosomal structure often lead to DNA damage, further exacerbating gene mutations and chromosomal rearrangements. However, the non­SMC condensin I complex subunit G (NCAPG) of the structural maintenance of chromosomes family is known to exert a key role in tumour development. It has been shown that high expression of NCAPG is closely associated with tumour development and progression. Overexpression of NCAPG variously affects chromosome condensation and segregation during cell mitosis, influences cell cycle regulation, promotes tumour cell proliferation and invasion, and inhibits apoptosis. In addition, NCAPG has been associated with tumour cell stemness, tumour resistance and recurrence. The aim of the present review was to explore the underlying mechanisms of NCAPG during tumour development, with a view towards providing novel targets and strategies for tumour therapy, and through the elucidation of the mechanisms involved, to lay the foundation for future developments in health.

NCAPG is transcriptionally regulated by CBX3 and activates the Wnt/ß-catenin signaling pathway to promote proliferation and the cell cycle and inhibit apoptosis in colorectal cancer.

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 (NCAPG) 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 NCAPG in CRC and its mechanism. Methods: Messenger RNA (mRNA) and protein expressions of NCAPG and chromobox protein homolog 3 (CBX3) 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/ß-catenin signaling-related proteins, and the activity of NCAPG 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 NCAPG expression was elevated in CRC cells. After transfection with sh-NCAPG, NCAPG expression was reduced. It was also discovered that NCAPG 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 CBX3 and NCAPG promoters. Meanwhile, the Encyclopedia of RNA Interactomes (ENCORI) database (https://starbase.sysu.edu.cn/) revealed that CBX3 was positively correlated with NCAPG. Our results showed that NCAPG was transcriptionally regulated by CBX3. Additionally, Wnt/ß-catenin signaling was discovered to be activated by CBX3 overexpression. Further experiments showed that NCAPG transcriptionally regulated by CBX3 activated Wnt/ß-catenin signaling to regulate the proliferation, cell cycle, and apoptosis of HCT116 cells. Conclusions: Collectively, the results of our study indicated that NCAPG was transcriptionally regulated by CBX3 and activated the Wnt/ß-catenin signaling pathway to facilitate the progression of CRC.