Chongfeng Sun

Cervical cancer cell-derived Tie1 expression via PI3K/AKT signaling pathway promotes tumor progression

Tie1 orphan receptor has become a focus of research, Tie1 can form a polymer with Tie2, regulate the Ang/Tie2 pathway and play a vital role in pathological angiogenesis and tumor progression, the function of Tie1 has remained uncertain in the progression of cervical cancer (CC). Here, we investigated the functional influences of Tie1 overexpress on CC in vitro and in vivo. We used Immunohistochemistry (IHC) analysis to detect the relative expression of Tie1 in CC, and we analyzed its connection with the overall survival (OS) and progression free survival (PFS)of CC patients. To prove the role of Tie1 in cell proliferation and metastatic, Tie1 expression in CC cell lines was upregulated by lentivirus. The high expression of Tie1 in tumor cells of cervical cancer tissues is significantly correlated with FIGO stage, differentiated tumors, tumors with diameters, deep stromal invasion. We found that cell progression was promoted in Tie1-overexpress CC cell lines in vivo and in vitro. Tie1 potentially exerts a commanding influence on the expression of markers associated with epithelial-mesenchymal transition (EMT) and the PI3K/AKT signaling pathway. Our research indicates that Tie1 is highly connected to CC progression as it may play a role in the EMT process through the PI3K/AKT signaling pathway.

LAMA5 promotes cell proliferation and migration in ovarian cancer by activating Notch signaling pathway

Abstract LAMA5 (laminin α5) is a member of the laminin family. Despite the recent research implicating LAMA5 in cancer, the function of LAMA5 has remained uncertain in the progression of ovarian cancer (OC). Here, we investigated the functional influences of LAMA5 knockdown on OC in vitro and in vivo. In this study, we used immunohistochemistry (IHC) analysis to detect the relative expression of LAMA5 in OC and non‐cancer tissues, and we analyzed its connection with the overall survival (OS) of OC patients. To prove the role of LAMA5 in cell proliferation, migration, and invasion, LAMA5 expression in OC cell lines was inhibited by lentivirus. Compared with normal fallopian tube tissue, epithelial ovarian cancer (EOC) tissue showe d critically higher LAMA5 expression levels; additionally, high LAMA5 levels were a poor predictor of OS. We found that cell progression was restrained in LAMA5‐knockdown OC cell lines in vivo and in vitro. Finally, LAMA5 might be a commanding inducer of the expression of epithelial‐mesenchymal transition (EMT) and Notch signaling pathway‐related markers. Together, our research indicates that LAMA5 is highly connected to OC progression as it may play a role in the EMT process through the Notch signaling pathway.

GSTO1 Promotes Cell Proliferation and Stemness of Cervical Cancer via Activating PI3K / AKT / mTOR Pathway

ABSTRACT Glutathione S‐transferase omega 1 (GSTO1) is overexpressed in a variety of cancers and plays an important role in the promotion of tumor proliferation and metastasis. Nevertheless, the function of GSTO1 in cervical cancer (CC) is unknown. Immunohistochemistry (IHC) was applied to observe GSTO1 protein levels in CC tissues. Cell proliferation, migration, and invasion capabilities were assessed using CCK8, EdU, plate cloning assays, and Transwell experiments in vitro. Flow cytometry was employed to analyze cell cycle progression and reactive oxygen species (ROS) levels. A subcutaneous xenograft model was utilized to observe cell growth in vivo. Cell stemness was assessed via sphere formation assay. Transcriptome sequencing and enrichment analysis were conducted to explore GSTO1‐related signaling pathways. The proteins linked to cell cycle regulation, stemness, epithelial‐mesenchymal transition (EMT), and the PI3K/AKT/mTOR signaling pathway were identified through western blotting and IHC. In this study, GSTO1 was highly expressed in CC tissues and associated with poor prognosis of patients. Knockdown of GSTO1 suppressed CC cell proliferation in vivo and in vitro and inhibited the cell cycle, stemness, migration, and EMT as in C1‐27 treatment. Conversely, down‐regulation of GSTO1 promoted ROS production in CC cells. RNA sequencing indicated that GSTO1 mediated the activation of the PI3K/AKT signaling pathway. In addition, silencing GSTO1 decreased the phosphorylation of PI3K, AKT, and mTOR proteins. Interestingly, 740 Y‐P (PI3K activator) reversed the inhibitory effects of GSTO1‐induced cell proliferation, cycle, stemness, and EMT via the PI3K/AKT/mTOR signaling axis. GSTO1 was important in CC progression through the PI3K/AKT/mTOR pathway and could serve as a promising therapeutic target.