MicroRNA-494-3p facilitates the progression of bladder cancer by mediating the KLF9/RGS2 axis.

Bladder cancer (BC) is a familiar malignancy with high morbidity and mortality. The effect of treatment is unsatisfactory after the metastasis and invasion of BC. Hence, more studies should be carried out to explore the metastasis of BC. RT-qPCR or/and western blot was conducted to evaluate miR-494-3p, KLF9, and RGS2 expression. Cell proliferation and invasion were estimated by MTT assay and transwell assay, respectively. Cell migration was tested by wound healing assay and transwell assay. Dual-luciferase reporter gene assay was employed to validate the interplay between miR-494-3p and KLF9 mRNA. The interaction between KLF9 and RGS2 promoter was verified using dual-luciferase reporter gene assay and chromatin immunoprecipitation (ChIP) assay. miR-494-3p expression was upregulated, whereas KLF9 and RGS2 were downregulated in BC cells. miR-494-3p inhibition was competent to limit the growth of BC cells. KLF9 knockdown abolished the miR-494-3p depletion-mediated inhibitory growth of BC cells. Mechanistically, we found that KLF9 was a downstream gene of miR-494-3p and could bind to the promoter region of RGS2 to promote the expression of RGS2. Moreover, RGS2 knockdown abrogated the suppressive effects of miR-494-3p knockdown on the proliferation, migration, and invasion of BC cells. Notably, miR-494-3p inhibition obstructed the tumor growth in nude mice. miR-494-3p silencing inhibited the progression of BC by regulating the KLF9/RGS2 axis in vitro and in vivo, which laid the foundation for experiments of miR-494-3p in BC and provided therapeutic targets for BC.

miR-145-5p Regulates the Proliferation, Migration and Invasion in Cervical Carcinoma by Targeting KLF5.

OBJECTIVE: Cervical carcinoma (CC) is a serious threat to women's health and few effective therapeutic methods have been discovered. The purpose of this study is to explore the underlying mechanism of miR-145-5p in CC. METHODS: Bioinformatics methods were employed to analyze the gene expression data of CC from TCGA database. qRT-PCR was used to detect the expression of miR-145-5p and KLF5 in CC cells, and Western blot was employed for the examination of KLF5 protein level. The targeted relationship between miR-145-5p and KLF5 was verified by a dual-luciferase reporter assay. Moreover, CCK-8, wound healing assay and transwell invasion assay were used to analyze the effects of miR-145-5p overexpression or KLF5 silencing on the proliferation, migration and invasion of CC cells. RESULTS: miR-145-5p was shown to be down-regulated in CC tissues and cells, while KLF5 was up-regulated. miR-145-5p could bind to the complementary sequence within the wild type KLF5 3'UTR rather than the mutant one. In addition, miR-145-5p could effectively down-regulate KLF5, in turn inhibiting the proliferation, migration and invasion of CC cells. CONCLUSION: miR-145-5p regulates the proliferation, migration and invasion of CC cells by targeting KLF5.

[Impact of diabetes mellitus on clinicopathological factors and relation with radiation pneumonitis in 332 patients with lung cancer].

OBJECTIVE: To explore the relation between diabetes mellitus and clinicopathological factors and the incidence of radiation pneumonitis in patients with non-small cell lung cancer. METHODS: The data of 332 patients with non-small cell lung cancer, who were admitted to the Department of Oncology of Third Xiangya Hospital of Central South University between January 2007 and August 2009, were collected retrospectively. The patients were divided into a diabetes mellitus (DM) group (n=45) and a non-diabetes mellitus (NDM) group (n=287). The clinicopathological factors were compared between the two groups. The patients who received radiotherapy were further divided into a diabetes mellitus (DMR) group (n=33) and a non-diabetes mellitus group (NDMR) group(n=287), and the incidence of radiation pneumonitis was compared. RESULTS: A total of 45 patients (13.55%)developed diabetes mellitus. There was significant difference in the body-weight, age and hypertension (P<0.05), while no significant difference in the pathologic factors, such as tumor pathological type, degree of differentiation, and classification of malignant tumors (TNM) stage between the two groups(P>0.05). No significant difference in the irradiation area was found between the DM group and the NDM group(P>0.05). The incidence of radiation pneumonitis in the DMR group was 42.42%(14 out of 33), while 21.31%(39 out of 183) in the NDMR group, with significant difference in the incidence of radiation pneumonitis between the DMR group and the NDMR group(P<0.05). The risk value in the DMR group was 2.721 folds (95%CI, 1.253-5.910) that in the NDMR group in patients with non-small cell lung cancer companied with diabetes mellitus. CONCLUSION: Diabetes mellitus is the risk factor of radiation pneumonitis for patients with nonsmall cell lung cancer who receive radiotherapy.