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.

Osteoarthritis (OA) is the most common joint disease in elderly individuals and seriously affects quality of life. OA has often been thought to be caused by body weight load, but studies have increasingly shown that OA is an inflammation-mediated metabolic disease. The current existing evidence suggests that OA is associated with obesity-related chronic inflammation as well as abnormal lipid metabolism in obesity, such as fatty acids (FA) and triglycerides. Adiponectin, a cytokine secreted by adipose tissue, can affect the progression of OA by regulating obesity-related inflammatory factors. However, the specific molecular mechanism has not been fully elucidated. According to previous research, adiponectin can promote the metabolism of FA and triglycerides, which indicates that it is a potential protective factor for OA through many mechanisms. This article aims to review the mechanisms of chronic inflammation, FA and triglycerides in OA, as well as the potential mechanisms of adiponectin in regulating chronic inflammation and promoting FA and triglyceride metabolism. Therefore, adiponectin may have a protective effect on obesity-related OA, which could provide new insight into adiponectin and the related mechanisms in OA.

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A facile method for the chemoselective reduction of graphene oxide (CrGO) has been developed via silver(I)-catalyzed decarboxylation. CrGO was characterized by X-ray photoelectron spectroscopy and X-ray diffraction. CrGO can be well-dispersed in most polar solvents, facilitating its nanosheet thin film preparation via a spin coating solution process for device fabrication. A proof of concept nonvolatile organic transistor memory device using CrGO as the charge-trapping layer showed a larger memory window of over 60 V and a higher ON/OFF current ratio of up to 10 4 compared to that of the precursor, graphene oxide (GO).decarboxylation of 1-naphthoic acid, elemental composition of GO, CGO and CrGO as determined by XPS, Raman and thermogravimetric analysis spectra, the output and transfer curves of GO and CrGO based organic nonvolatile memory transistors. See