NCAPG2 (Non-SMC Condensin II Complex Subunit G2)

PBK is a key regulator of pancreatic cancer and interacts with NCAPG2 to promote tumor progression, suggesting its value as a potential biomarker and therapeutic target for pancreatic cancer.

High expression of RPL35A is linked to poor prognosis in hepatocellular carcinoma. The regulation of NCAPG2 by RPL35A may represent a critical mechanism underlying RPL35A-driven tumor progression. Targeting the RPL35A/NCAPG2 pathway may offer a promising therapeutic strategy for HCC treatment.

Current research indicates that NCAPG2 may provide effective assistance for the early diagnosis and pathological classification of CHOL, potentially regulating the immune microenvironment and thereby influencing the occurrence and progress of CHOL.

In addition, knockdown of NCAPG2 reduced the resistance of gastric adenocarcinoma cells to albumin-bound paclitaxel and down-regulated STAT3 and NF-κB signaling pathways. In summary, NCAPG2 plays an important role in the malignant progression of gastric adenocarcinoma and is involved in the resistance to albumin-bound paclitaxel.

Notably, although the condensin II subunits (ncaph2, ncapg2, and ncapd3) were essential for HSPC maintenance, the condensin I subunits did not affect HSPC development. These findings emphasize the crucial role of condensin II in ensuring healthy hematopoiesis via promoting HSPC proliferation.

The study emphasizes the potential importance of NCAPG, NCAPG2, and NCAPH in ACC, suggesting roles in tumor aggressiveness and diagnostic relevance. These genes could serve as therapeutic targets and markers for ACC, but further exploration into their molecular activities and validation studies is imperative to fully harness their diagnostic and therapeutic potential, advancing precision medicine approaches against this rare but lethal malignancy.

Furthermore, an interaction between RACGAP1 and the subunit G2 of the condensin II complex, known as non-SMC condensin II complex subunit G2 (NCAPG2), has been identified. Our findings may provide new insight for improving therapeutic strategies for OV.

The higher the expression of MYC and NCAPG2, the worse the prognosis. MYC and NCAPG2 are core molecules in gastric cancer.

High MYC and NCAPG2 expression has been observed in colorectal cancer, and increased MYC and NCAPG2 expression correlates with worse prognosis.

NCAPG2 is highly expressed in PCa, and its level is significantly associated with PCa prognosis. NCAPG2 promotes PCa malignancy and drives cancer stemness via the STAT3/c-MYC signaling axis, highlighting its potential as a therapeutic target for PCa.

Publicly available databases and various bioinformatics tools were used to study the heterogeneity of cuproptosis in patients with HCC. Three HCC subtypes were identified, with differences in the survival outcomes, genomic instability, senescence environment, and response to anticancer drugs. Further, three cuproptosis-related genes were identified, which could be used to design personalized therapeutic strategies for HCC.

We highlighted that miR-638 suppresses cervical cancer progression by inhibiting NCAPG2 under tetrandrine treatment.