PHB2 (Prohibitin 2)

Our findings establish Src-mediated PHB2 phosphorylation as a redox-sensitive molecular switch that drives HCC metabolic reprogramming by disrupting the PHB2-cardiolipin cristae axis. This phosphorylation event represents a targetable vulnerability for this malignancy with limited treatment options.

In conclusion, PHB2 exhibits cancer-type-specific prognostic associations. Its overlapping mutation and modification sites suggest potential functional importance, supporting its role as a candidate biomarker for further validation in pan-cancer contexts.

In microglia differentiation, SOCS1 and PHB2 showed dynamic expression patterns. These findings provide new strategies for GBM prognosis and treatment.

Our findings revealed that PHB2 knockdown decreased glioma malignant phenotypes and radio-resistance by inhibiting mitophagy via PARL-PGAM5-PINK1-Parkin pathway. PHB2 is a promising candidate target for the development of new therapeutic strategy to enhance the efficacy of radiotherapy for glioma.

Further mechanistic investigation reveals that PHB2 enhances NOX1 transcription by interacting with the transcription factor C/EBP-beta and promoting its translocation into the nucleus, resulting in elevated intracellular oxidative signaling driven by NOX1, which subsequently activates ERK. Therefore, we propose that targeting PHB2-C/EBP-beta-NOX1-mediated cytosolic oxidative stress could offer a promising therapeutic avenue for combating gastric cancer malignant progression.

Furthermore, in vitro and in vivo experiments showed that inhibition of PART1 confers resistance to both cisplatin and PARP inhibitor and promotes cellular senescence...PDX models were utilized to further confirm the findings. Altogether, our study demonstrated that lncRNA PART1 has the potential to serves as a novel promising target to reverse resistance to PARPi and improve prognosis in ovarian cancer.

Improvement of erythropoiesis that accompanies NLK inhibition is negated when TFAM and PHB2 upregulation is prevented. These data demonstrate that a significant contribution of NLK on the pathogenesis of DBA is through loss of mitochondrial biogenesis.

Prx1Cys52 functions as a redox sensor that binds to PHB2 and regulates mitophagy in the senescence of OLK, suggesting its potential as a clinical target.

These observations indicate that GOLPH3 is a negative regulator of ferroptosis in CRC cells. GOLPH3 protects these cells from ferroptosis by inducing the expression of PHB1 and PHB2, and by interacting with PHB2 and NRF2.

lncRNA BLACAT1 is highly expressed in HSCC tumor tissues and plays a crucial role in the development of HSCC in vitro and in vivo. This increased expression may be caused by STAT3/AKT pathway activation, consequently inhibiting P21 expression through PHB2.

After in vivo injection of PHB2 with deletion of NIS (rΔNIS-PHB2), the nuclear translocation of STAT did not change significantly compared to that in the control group. These results suggest that PHB2 promoted the nuclear translocation of STAT through NIS and mediated the expression of antiviral proteins to inhibit WSSV infection.

Our findings highlight the importance of PHB2 upregulation in driving GC progression and its association with adverse patient outcomes. Understanding the functional impact of PHB2 on GC growth contributes valuable insights into the molecular underpinnings of GC and may pave the way for the development of targeted therapies to improve patient outcomes.