NCAPH (Non-SMC Condensin I Complex Subunit H)

The sensitivity of LGG patients with high NCAPH expression to chemotherapy agents such as temozolomide also suggests the potential therapeutic effect of chemotherapy combined with immunotherapy. Furthermore, NCAPH was positively correlated with cell cycle, proliferation, DNA damage and repair, EMT, invasion, and apoptosis, while negatively associated with inflammation, quiescence and angiogenesis. Together, this study provides a comprehensive understanding of the role of NCAPH in LGG and suggests that NCAPH may be a potential prognostic biomarker for LGG patients, with potential for drug development and immunotherapy.

This study identifies NCAPH as a novel oncogenic factor in BC. NCAPH interacts with YAP1, promoting its nuclear translocation and enhancing BCSC traits and malignancy. Critically, YAP1 inhibition reverses NCAPH-driven effects, validating the NCAPH as a promising therapeutic target.

Individuals with ccRCC who demonstrated elevated levels of NCAPH were at an increased likelihood of experiencing poor prognostic outcomes. Moreover, NCAPH was crucial for promoting cellular growth and inhibiting apoptosis by activating the PI3K/AKT signaling pathway in ccRCC, suggesting its potential utility as both a marker for prognosis and a target for therapy.

This study showed that NCAPH can serves as a novel potential oncogenic biomarker for LUSC and its regulation is controlled by upstream miR-1976. miR-1976 can directly targets NCAPH to affect the proliferation, migration, invasion, and apoptosis of LUSC cell.

Collectively, silencing NCAPH impedes malignant progression of ovarian cancer through modulation of the MEK/ERK/PD-L1 pathway.

Notably, combining NCAPH knockdown with an mTOR inhibitor (Everolimus) or a cyclin-dependent kinase inhibitor (Flavopiridol) demonstrated promising anti-tumor effects both in vitro and in vivo. This study highlights the significant pro-tumor role of NCAPH in PCa and suggests its potential as a therapeutic target.

Taken together, circEIF3I elevated NCAPH expression by sponging miR-328-3p, thereby promoting CRC metastasis. These findings suggest that the circEIF3I/miR-328-3p/NCAPH axis represents a novel therapeutic target for CRC.

We identified and validated high tissue levels of NCAPH, UBE2C, and ZWINT as novel prognostic risk factors in clinically localized PCa patients. The use of these markers can improve routinely used risk estimation models.

In a TNBC cell-derived xenograft model, ZCCHC3-specific siRNA injection successfully reduced in vivo TNBC tumor growth and downregulated NCAPH expression. Overall, our findings demonstrate that ZCCHC3 and Efp coordinately promote TNBC progression by regulating NCAPH expression and that ZCCHC3/Efp/NCAPH pathway can be applied to clinical TNBC management.

Therefore, we provide evidence for the role of the TRIM21-NCAPH axis in cervical cancer autophagy and proliferation and the involvement of the AKT/mTOR signaling pathway in this process. These results deepen our understanding of the carcinogenesis of cervical cancer, broaden the understanding of the molecular mechanisms of TRIM21 and NCAPH, and provide guidance for individualized treatment of cervical cancer in the future.

NCAPH has the ability to form complexes with other proteins that are involved in glycolysis, DNA damage repair, and chromatin remodeling. This review indicates that NCAPH expression in most malignant tumors is associated with poor prognosis and low recurrence-free survival.

In conclusion, miR-1976 inhibits NCAPH activity in LUAD and acts as a tumor suppressor. The miR-1976/NCAPH/NF-κB axis may, in the future, represent crucial diagnostic and prognostic biomarkers and promising therapeutic options.