Retracted: MicroRNA‐92a promotes tumor growth and suppresses immune function through activation of MAPK/ERK signaling pathway by inhibiting PTEN in mice bearing U14 cervical cancer

Abstract Cervical cancer is known as the possible outcome of genital infection, while the molecular mechanisms of initiation, development, and metastasis of cervical cancer have not yet been fully elucidated. Our study aims to investigate the effects of microRNA‐92a (miR‐92a) on tumor growth and immune function by targeting PTEN via the MAPK/ERK signaling pathway in tumor‐bearing mice. C57BL/6 female mice were used for tumor‐bearing mouse models and their tumor and adjacent normal tissues were collected, and normal cervical tissues were obtained from normal mice. Serum levels of tumor necrosis factor‐α (TNF‐α) and soluble interleukin‐2 receptor (sIL‐2R) were detected by ELISA. The cells were divided into the normal, blank, negative control (NC), miR‐92a mimic, miR‐92a inhibitor, siRNA‐PTEN, and miR‐92a inhibitor + siRNA‐PTEN groups. Dual‐luciferase reporter assay was adopted to determine the relationship between PTEN and miR‐92a. Expressions of miR‐92a, PTEN, TNF‐α, sIL‐2R, ERK1, and ERK2 were tested by RT‐qPCR and Western blotting. Cell proliferation was detected by cell count kit‐8 (CCK‐8); cell cycle and apoptosis were detected by flow cytometry. Compared with the normal cervical tissues and adjacent normal tissues, the cervical cancer tissues exhibited increased expressions of miR‐92a, p‐ERK1/2, and serum levels of TNF‐α and sIL‐2R while decreased PTEN expression. PTEN was confirmed to be the target gene of miR‐92a. As compared with the blank and NC groups, expressions of miR‐92a, ERK1 and ERK2 increased, and expressions of PTEN decreased in the miR‐92a mimic group. The miR‐92a mimic group exhibited increased expression levels of TNF‐α and sIL‐2R, cell proliferation, and cell number in S phase but decreased cell apoptosis, and cell number in G0/G1 phase, while the miR‐92a inhibitor group followed opposite trends. miR‐92a promotes tumor growth and suppresses immune function by inhibiting PTEN via activation of the MAPK/ERK signaling pathway in mice bearing U14 cervical cancer