Long non-coding RNA LINC00992 promotes hepatocellular carcinoma cell proliferation, metastasis, and invasiveness by downregulating MicroRNA miR-361-5p expression to increase levels of the transcription factor twist1.

Hepatocellular carcinoma (HCC) is one of the most common cancers, and has an extremely poor prognosis. Our previous study confirmed that the microRNA miR-361-5p inhibited the proliferation, metastasis, invasiveness, and epithelial-to-mesenchymal transition (EMT) process of HCC by targeting the transcription factor Twist1. Long non-coding RNAs (lncRNAs) are key regulators of processes such as cell differentiation, inflammation, tumor formation, and immune escape.

MicroRNA-361-5p Inhibits Tumorigenesis and the EMT of HCC by Targeting Twist1.

MicroRNA-361-5p (miR-361-5p) is a tumor suppressor miRNA that is dysregulated in several types of human cancer. However, the functional significance of miR-361-5p in hepatocellular carcinoma (HCC) is unclear. This study explored the biological function of miR-361-5p in regulating the progression of HCC and the underlying molecular mechanism.

Relation between Ki-67, ER, PR, Her2/neu, p21, EGFR, and TOP II-α expression in invasive ductal breast cancer patients and correlations with prognosis.

The aim of the present study was to investigate the expression of the transcription factor Ki-67, ER, PR, Her2/neu, p21, EGFR, and TOP II-α in the tumor tissue of patients with invasive ductal carcinoma(IDC); in addition, we examined correlations between these markers. Two hundred and sixteen IDC patients, who were not previously been treated with chemo- or radiotherapy, were included in the study. All tumors were grade I-III.

Prevalence and clinical relevance of T-helper cells, Th17 and Th1, in hepatitis B virus-related hepatocellular carcinoma.

Background And Aims: An immune imbalance in the cytokine profile exerts a profound influence on the progression of hepatitis B virus (HBV) infections and hepatocellular carcinoma (HCC). The present study evaluated the immune status of T helper (Th) 17 and Th1 cells in patients with HBV-related and non-HBV-related HCC.

Methods: We randomly enrolled 150 patients with HCC.