Abstract
We investigated the effects of Pseudomonas aeruginosa mannose-sensitive hemagglutinin (PA-MSHA) on the proliferation and invasion of human cervical cancer cell lines, as well as the molecular pathways underlying these effects. MTT cell proliferation assays revealed a time- and concentration-dependent cytotoxic effect of PA-MSHA on HeLa cells but not H8 cells. Flow cytometry with propidium iodide and annexin-V-fluorescein isothiocyanate labeling (FITC) indicated that various concentrations of PA-MSHA could induce apoptosis and G2-M cell cycle arrest in HeLa cells. PA-MSHA also impaired the migration and invasion abilities of HeLa cells in Wound healing and Transwell invasion assays. Western blot results demonstrated that PA-MSHA reduced the expression of p-AKT, p-GSK3β, BCL-2, Vimentin and β-catenin, but increased the levels of PTEN, BAD, BAX and E-cadherin in HeLa cells. Importantly, PTEN siRNA induced the activity of p-AKT, while PA-MSHA partly inhibited this induction, indicating that PA-MSHA may reduce the cell proliferation and invasion potential by activating PTEN and thus inhibiting the AKT pathway in vitro. These data suggest the potential application of PA-MSHA to the treatment of human cervical cancer.
Highlights
Cervical cancer is a major malignancy of the female genital tract that can spread to adjacent organs and to the pelvic and para-aortic lymph nodes
The MTT assay revealed that exposure of human cervical carcinoma (HeLa) cells to Pseudomonas aeruginosa mannose-sensitive hemagglutinin (PA-MSHA) for up to 72 h had a cumulative concentration- and time-dependent inhibitory effect on cell proliferation (Figure 1A and 1B)
Because P. aeruginosa (PA)-MSHA inhibited the proliferation of HeLa cells, we investigated the mechanism by which PA-MSHA suppressed growth
Summary
Cervical cancer is a major malignancy of the female genital tract that can spread to adjacent organs and to the pelvic and para-aortic lymph nodes. The rate of cervical cancer has declined since 1960, this disease is still a major burden in the Asia-Pacific region [2]. HPV infection alone is not sufficient to transform epithelial host cells to cancer cells. Other factors, such as the upregulation of oncogenes and the aberrant activation of related signaling pathways, could be involved in cervical carcinogenesis. Three methods are commonly used to treat cervical cancer: surgery, chemotherapy and radiation therapy. Recent research has demonstrated that engineered bacteria can be used to treat cancer [4], and the development of a new treatment method for cervical cancer is feasible
Sign-in/Register to view highlights & summary Sign-in/Register to access full text options 
Free) 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a call
