Dongdong Wu

Cystathionine‐γ‐Lyase/Hydrogen Sulfide Axis Plays a Crucial Role in Promoting the Progression of Cervical Cancer

ABSTRACT The role of endogenous hydrogen sulfide (H 2 S) in the pathophysiological mechanisms of various organ tumors has been extensively studied; however, its relevance to cervical cancer remains unexplored. This study aimed to examine the effect of endogenous H 2 S and its main synthetic enzyme, cystathionine‐γ‐lyase (CSE), in regulating the growth behavior in cervical cancer cells. The proliferation, migration, and invasion of C33A and HeLa cervical cancer cells were investigated, followed by molecular, biochemical, and immunocytochemical analyses. The results indicated that CSE is highly expressed in C33A and HeLa cells and modulates the levels of endogenous H 2 S. CSE knockdown suppressed the proliferation, migration, and invasion of cervical cancer cells. The CSE‐mediated growth patterns involved epithelial–mesenchymal transition (EMT), mitochondrial apoptosis, pyroptosis, reactive oxygen species (ROS) production, and the PI3K/AKT/mTOR signaling pathway. Additionally, CSE knockdown inhibited the growth of xenograft tumors in vivo. Similarly, CSE overexpression was performed for reverse verification. In brief, inhibition of CSE reduced cervical cancer growth, while overexpression of CSE promoted it. These findings indicated that CSE may serve as a potential target for early diagnosis, prognosis assessment, and therapeutic intervention in cervical cancer.

PCNP promotes ovarian cancer progression by accelerating β‐catenin nuclear accumulation and triggering EMT transition

AbstractEver reports showed that PCNP is associated with human cancers including neuroblastoma and lung cancer. However, the role and underlying molecular mechanism of PCNP in ovarian cancer have not been plenty elucidated. Herein, we first investigated the expression of PCNP in ovarian cancer tissues and cells, the effects of PCNP in ovarian cancer proliferation, apoptosis, migration and invasion, and determined the molecular mechanism of PCNP in ovarian cancer progression. The results indicated that PCNP was significantly overexpressed in human ovarian cancer tissues and cells, and related to poor prognosis in ovarian cancer patients. In addition, we also detected that PCNP promoted ovarian cancer cells growth, migration and invasion, as well as inhibited ovarian cancer cells apoptosis. Mechanistically, PCNP binding to β‐catenin promoted β‐catenin nuclear translocation and further activated Wnt/β‐catenin signalling pathway. Moreover, PCNP regulated the expression of genes involved in EMT and further triggered EMT occurrence. Conclusionally, PCNP may promote ovarian cancer progression through activating Wnt/β‐catenin signalling pathway and EMT, acting as a novel and promising target for treating ovarian cancer.