Knockdown of ACTA2­AS1 promotes liver cancer cell proliferation, migration and invasion.

Long noncoding RNAs (lncRNAs) are important regulators of various cellular and biological processes. The present study aimed to investigate the functions of a novel lncRNA, ACTA2­AS1:4, a transcript variant of smooth muscle α­actin 2­antisense 1 (ACTA2­AS1), in regulating liver cancer progression. Expression of lncRNAs in liver cancer tissues and cell lines were analyzed by reverse transcription quantitative polymerase chain reaction (RT­qPCR). Knockdown of ACTA2­AS1:4 expression in LM3 liver cancer cells was achieved by transfection with small interfering RNAs (siRNAs) that specifically targeted ACTA2­AS1:4. The proliferation and cell cycle progression of ACTA2­AS1:4­silenced LM3 cells were determined using MTS assay and flow cytometry, respectively. A Transwell system assay was used to evaluate the migration and invasion capacities of LM3 cells transfected with ACTA2­AS1:4 siRNA. The expression levels of major genes associated with important cellular processes were finally determined by RT­qPCR and western blot analysis. ACTA2­AS1:4 expression in liver cancer tissues and multiple cell lines was markedly downregulated by specific siRNAs. This inhibition of ACTA2­AS1:4 expression significantly promoted the proliferation, cell cycle progression, migration and invasion of LM3 cells. A decrease in ACTA2­AS1:4 expression also suppressed E­cadherin expression, increased N­cadherin expression, decreased caspase 3 expression and increased cyclin D1 and matrix metalloproteinase expression in liver cancer cells. Downregulation of ACTA2­AS1:4 affects a number of key mechanisms involved in liver cancer progression. These data may be important for the future of liver cancer diagnosis and subsequent treatments.

UNBS5162 inhibits colon cancer growth via suppression of PI3K/Akt signaling pathway.

Colon cancer is a common cause of cancer-related death worldwide. However, the underlying mechanism of tumor progression of colon cancer remains far from being elucidated. In the present study, we report the role of UNBS5162 in colon cancer. UNBS5162 is a naphthalimide that can intercalate into DNA and suppress the expression level of CXCL chemokines. Here, we investigated its effect on cell proliferation, mobility and apoptosis in HCT116 cells, and explored the underlying mechanism. A CCK8 assay revealed that UNBS5162 can block the proliferation of colon cancer cells. Base on a Transwell assay, we showed that cell migration and invasion ability of HCT116 cells are inhibited by UNBS5162. In addition, Annexin V-FITC/PI assay and Western blot analysis were performed to detect whether UNBS5162 could induce cell apoptosis. The results indicated that UNBS5162 increases the number of apoptotic cells remarkably. Furthermore, Western blot analysis demonstrated that UNBS5162 down-regulates the expression level of Bcl2, and up-regulates that of Bax as well as the level of activated Caspase-3. Moreover, we examined the impact of UNBS5162 on PI3K/Akt signaling pathway. UNBS5162 substantially inhibited the phosphorylation of Akt and its downstream effector mTOR, and reduced the expression of p-70. Taken together, these results suggest that UNBS5162 should be considered as a potent therapeutic anticancer agent that targets the PI3K/AKT signaling pathway.

Long non-coding RNA LINC00673 promotes hepatocellular carcinoma progression and metastasis through negatively regulating miR-205.

Increasing evidence demonstrates abnormal expression of long non-coding RNA (lncRNA) is closely correlated with various malignancies including hepatocellular carcinoma (HCC). The present study aims to investigate the role of lncRNA long intergenic noncoding RNA 00673 (LINC00673) in tumorigenesis of HCC. Quantitative real-time polymerase chain reaction (qRT-PCR) revealed LINC00673 was upregulated in HCC cancerous tissue and cell lines compared to adjacent normal tissue and normal liver cell lines. LINC00673 overexpression is associated with poor prognosis and low survival rate. LINC00673 silencing inhibited the proliferation, invasion and epithelial-mesenchymal transition (EMT) of HCC cells in vitro. Bioinformatics analysis revealed that miR-205 targeted 3'-UTR of LINC00673. Rescue experiments confirmed that miR-205 could reverse the effect of LINC00673 on HCC cells. In vivo xenograft tumor assay LINC00673 silencing reduced the tumor volume and weight. Taken together, findings indicate overexpression of LINC00673 promotes HCC cells progression by regulating miR-205, providing a prognostic biomarker and therapeutic target for HCC and is associated with poor survival of HCC patients.