PMID- 37201048
OWN - NLM
STAT- PubMed-not-MEDLINE
LR  - 20230521
IS  - 2078-6891 (Print)
IS  - 2219-679X (Electronic)
IS  - 2078-6891 (Linking)
VI  - 14
IP  - 2
DP  - 2023 Apr 29
TI  - NCAPG is transcriptionally regulated by CBX3 and activates the Wnt/beta-catenin 
      signaling pathway to promote proliferation and the cell cycle and inhibit 
      apoptosis in colorectal cancer.
PG  - 900-912
LID - 10.21037/jgo-23-63 [doi]
AB  - 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/beta-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/beta-catenin signaling was discovered to be 
      activated by CBX3 overexpression. Further experiments showed that NCAPG 
      transcriptionally regulated by CBX3 activated Wnt/beta-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/beta-catenin signaling pathway to facilitate 
      the progression of CRC.
CI  - 2023 Journal of Gastrointestinal Oncology. All rights reserved.
FAU - Yang, Hong
AU  - Yang H
AD  - Department of Gastroenterology, Digestive Disease Hospital, Affiliated Hospital 
      of Zunyi Medical University, Zunyi, China.
FAU - Pu, Leilei
AU  - Pu L
AD  - Department of Gastroenterology, Digestive Disease Hospital, Affiliated Hospital 
      of Zunyi Medical University, Zunyi, China.
FAU - Li, Ruobing
AU  - Li R
AD  - Department of Gastroenterology, Digestive Disease Hospital, Affiliated Hospital 
      of Zunyi Medical University, Zunyi, China.
FAU - Zhu, Rong
AU  - Zhu R
AD  - Department of Gastroenterology, Digestive Disease Hospital, Affiliated Hospital 
      of Zunyi Medical University, Zunyi, China.
LA  - eng
PT  - Journal Article
DEP - 20230227
PL  - China
TA  - J Gastrointest Oncol
JT  - Journal of gastrointestinal oncology
JID - 101557751
PMC - PMC10186512
OTO - NOTNLM
OT  - Colorectal cancer (CRC)
OT  - Wnt/beta-catenin signaling
OT  - chromobox protein homolog 3 (CBX3)
OT  - non-structural maintenance of chromosomes condensin I complex subunit G (NCAPG)
COIS- Conflicts of Interest: All authors have completed the ICMJE uniform disclosure 
      form (available at 
      https://jgo.amegroups.com/article/view/10.21037/jgo-23-63/coif). The authors have 
      no conflicts of interest to declare.
EDAT- 2023/05/18 19:12
MHDA- 2023/05/18 19:13
PMCR- 2023/04/29
CRDT- 2023/05/18 16:54
PHST- 2023/01/03 00:00 [received]
PHST- 2023/02/16 00:00 [accepted]
PHST- 2023/05/18 19:13 [medline]
PHST- 2023/05/18 19:12 [pubmed]
PHST- 2023/05/18 16:54 [entrez]
PHST- 2023/04/29 00:00 [pmc-release]
AID - jgo-14-02-900 [pii]
AID - 10.21037/jgo-23-63 [doi]
PST - ppublish
SO  - J Gastrointest Oncol. 2023 Apr 29;14(2):900-912. doi: 10.21037/jgo-23-63. Epub 
      2023 Feb 27.