MiR-3194-3p Inhibits Breast Cancer Progression by Targeting Aquaporin1.

Increasing evidence indicates that the Aquaporin1 (AQP1) aberrant expression may be related to a wide variety of human cancers, including breast cancer (BC). In the present study, we explore the effects and possible mechanism of miR-3194-3p on the biological behaviors of BC. At first, miR-3194-3p is found to modulate expression targeting the 3'-UTR using miRNA target prediction algorithms.

Decreased expression of aquaporin 1 correlates with clinicopathological features of patients with cervical cancer.

We aimed to investigate the expression dynamics of Aquaporin 1 () in cervical cancer and evaluate correlations among levels and the clinicopathological features of patients with cervical cancer. mRNA and protein levels in cervical cancer and adjacent normal tissues were evaluated by quantitative reverse-transcription PCR (qRT-PCR) and western blot. Immunohistochemistry (IHC) for was performed with a tissue microarray of cervical cancer (containing 63 cases of squamous cell cervical cancers and 10 normal cervical tissues) to investigate clinicopathological outcomes.

[RNA interference of HERC4 inhibits proliferation, apoptosis and migration of cervical cancer Hela cells].

Objective: To explore the effects of silencing HERC4 on the proliferation, apoptosis, and migration of cervical cancer cell line Hela and the possible molecular mechanisms.

Methods: Three HERC4-specific small interfering RNAs (siRNAs) were transfected into Hela cells, and HERC4 expression in the cells was examined with Western blotting. CCK-8 assay, annexin V-FITC/PI assay, and wound healing assay were used to assess the effect of HERC4 silencing on the proliferation, apoptosis and migration ability of Hela cells.

Decreased expression of Sushi Domain Containing 2 correlates to progressive features in patients with hepatocellular carcinoma.

Background: Sushi Domain Containing 2 (SUSD2) has been identified as a regulator of colon and breast cancer. Increasing evidence suggests that SUSD2 plays a key role in tumorigenesis. However, the SUSD2 expression status and its functions in hepatocellular carcinoma (HCC) are still unrevealed.

Reduced expression of sushi domain containing 2 is associated with progression of non-small cell lung cancer.

Sushi domain containing 2 (SUSD2) has been identified as a gene encoding an 822-amino acid protein, which contains a transmembrane domain and functional domains inherent to adhesion molecules. Previous studies have reported that increased expression of SUSD2 has a critical role in tumorigenesis in human breast cancer. However, to the best of our knowledge, SUSD2 expression status and its correlation with the clinicopathological features of non-small cell lung cancer (NSCLC) have not previously been investigated.

Association between hepatitis B virus infection and diabetes mellitus: A meta-analysis.

Hepatitis B virus (HBV) infection has been shown by certain studies to be associated with diabetes mellitus (DM); however, the results of these studies were controversial. For that reason, a meta-analysis of the literature was performed in order to determine the association between HBV infection and the prevalence of DM more accurately. The PubMed, Embase, Chinese National Knowledge Infrastructure and Wan Fang databases, as well as the Chinese Science and Technology Journal Database, were searched for literature published until June 2014.

MiR-204-5p/Six1 feedback loop promotes epithelial-mesenchymal transition in breast cancer.

Epithelial-mesenchymal transition (EMT) is a vital process in epithelial cancer invasion and metastasis. The induction of EMT by Six1 has been described as a common mode of cancer progression, which could promote breast cancer migration and invasion. In the study, we found that miR-204-5p could suppress the migration and invasion of breast cancer cell lines.

Increased expression of Six1 correlates with progression and prognosis of prostate cancer.

Sineoculis homeobox homolog 1 (Six1), normally a developmentally restricted transcriptional regulator, is frequently dysregulated in mutiple cancers. Increasing evidences show that overexpression of Six1 plays a key role in tumorigenesis. However, the Six1 expression status and its relationship with the clinicopathological characteristics in prostate cancer were unclear.