Role And Mechanism Of ALOX12B In The Progression Of Cervical Cancer

Purposes:Cervical cancer is a malignant disease and a big threat for women worldwide.Surgical resection or concurrent radiochemotherapy is the main strategy for cervical cancer.But some patients with advanced tumor could not benefit from those traditional therapies,which results in poor clinical outcome.ALOX12 B is a gene encoding lipoxygenase and mutation in ALOX12 B was detected in lung and breast cancer.Furthermore,ALOX12 B was essential to proliferation of epidermoid carcinoma cells.However,the role of ALOX12 B in cervical cancer has not been reported,so it is necessary to study the role and mechanism of ALOX12 B in cervical cancer Methods:To study the function of ALOX12 B in the development of cervical cancer,we reduced the expression of ALOX12 B in the cervical cancer cell lines ca-ski and C33 A by lentiviral vector.q-PCR was used to detect the knockdown efficiency of the virus to ALOX12 B.We designed CCK-8 and clone formation experiments to verify the effect of knockdown of ALOX12 B on the proliferation and clone formation of cervical cancer cells.PI detection was used to verify the effect of ALOX12 B knockdown on the cell cycle of cervical cancer.We tested the effect of ALOX12 B on the migration and invasion of tumor cells by transwell and wound healing experiments in vitro.In addition,we designed a xenograft model to further verify the role of ALOX12 B in the development of cervical cancer in vivo.To further elucidate the role of ALOX12 B in the development of cervical cancer,we predicted the target of ALOX12 B through literature research and database analysis.Western blot was used to detect whether ALOX12 B promoted the expression of PTGS2.In addition,the rescue test examined whether PTGS2 could regulate the promoter action of ALOX12 B on the proliferation of cervical cancer cells.Results:CCK-8 and clone formation assay showed that the proliferation and clone formation ability of cervical cancer cells were significantly impaired after ALOX12 B knockdown.In addition,PI detection showed that the cell cycle of cervical cancer cells was blocked in G1 phase after knockdown of ALOX12 B.Xenograft tumor model showed that ALOX12 B knockdown could significantly inhibit the growth of cervical cancer tumors.In addition,Transwell and wound healing experiments showed that ALOX12 B had no significant effect on the migration and invasion of tumor cells in vitro,while Western blot analysis showed that ALOX12 B could regulate the expression of tumor EMT-related proteins(Vimentin,N-cadherin and E-cadherin)in vivo.We speculate that,unlike in vitro experiments,the function of ALOX12 B in cervical cancer tumor tissues may be related to the hypoxic environment of cervical cancer tumor tissues.We predict that PTGS2 may be one of the main targets of ALOX12 B through literature research and database analysis.Western blot showed that ALOX12 B knockdown could significantly inhibit the expression of PTGS2.In addition,the rescue experiment showed that PTGS2 could regulate the promoter action of ALOX12 B on the proliferation of cervical cancer cells.Conclusion:Our study reported the role of ALOX12 B in the development of cervical cancer,and ALOX12 B may regulate the progression of cervical cancer through PTGS2.This study will provide theoretical guidance for the new treatment of cervical cancer patients.