Pontibaca salina sp. nov., isolated from marine sediment.

A Gram-stain-negative, oval or short rod-shaped, non-motile, aerobic bacterium, designated strain S1109LT, was isolated from a marine sediment in Weihai, PR China. Cells were oxidase positive and catalase positive. Growth of strain S1109LT occurred at 10-40 °C (optimum, 30-33 °C), pH 6.5-10.0 (optimum, 7.0-8.0) and in the presence of 1-21% (optimum, 4-6%) (w/v) NaCl. 16S rRNA gene sequence phylogeny indicated that strain S1109LT was associated with the genus Pontibaca of the family Rhodobacteraceae because it showed the highest sequence similarity to Pontibaca methylaminivorans KCTC 22497T (97.5%). The average nucleotide identity (ANI) and the digital DNA-DNA hybridization (dDDH) scores between strain S1109LT and Pontibaca methylaminivorans KCTC 22497T were 74.6% and 18.7%. The major cellular fatty acids of strain S1109LT were C19:0 cyclo ω8c and C18:1 ω7c. The polar lipids profiles of strain S1109LT were phosphatidylglycerol, phosphatidylcholine, phosphatidylethanolamine and two unidentified lipids. Strain S1109LT contained ubiquinone-10 as the major respiratory quinone. The genomic DNA G + C content was 55.9 mol%. On the basis of the evidence presented in this study, strain S1109LT is considered to represent a novel species of the genus Pontibaca, for which the name Pontibaca salina sp. nov. is proposed. The type strain of is S1109LT (= KCTC 82411T = MCCC 1H00441T).

LncRNA ANCR Suppresses the Progression of Hepatocellular Carcinoma Through the Inhibition of Wnt/ß-Catenin Signaling Pathway.

OBJECTIVE: Our study aimed to investigate the effect of anti-differentiation noncoding RNA (ANCR) on hepatocellular carcinoma (HCC) and its potential molecular mechanisms. METHODS: The expression of ANCR was detected by qRT-RCR in both HCC tissues and HCC cells. Moreover, the relationship between ANCR expression and clinical parameters in HCC patients was investigated. The proliferation, cell clones, migration, invasion and apoptosis of MHCC97H and HCCLM3 cells were measured by MTT assay, colony formation assay, transwell assay and flow cytometry, respectively. The expressions of N-cadherin, vimentin, E-cadherin, cleaved caspase-3, Bax, Bcl-2, Wnt1, ß-catenin and GSK-3ß in MHCC97H and HCCLM3 cells were measured by Western blot. RESULTS: Our results showed that ANCR was lowly expressed in both HCC tissues and HCC cells. ANCR expression was closely associated with tumor size, tumor-node-metastasis (TNM) stages and vascular invasion in HCC. ANCR could dramatically inhibit cell proliferation, migration and invasion, as well as promote apoptosis in MHCC97H and HCCLM3 cells. ANCR could significantly increase the expression of cleaved caspase-3, Bax, E-cadherin and GSK-3ß but reduce the expression of Bcl-2, N-cadherin, vimentin, Wnt1 and ß-catenin in MHCC97H and HCCLM3 cells. In addition, Wnt/ß-catenin pathway inhibitor (IWP-2) partially reversed the effects of silencing ANCR on the proliferation, migration, invasion and apoptosis of HCCLM3 cells. CONCLUSION: Our study demonstrated that ANCR can suppress cell proliferation, migration and invasion, as well as promote apoptosis of HCC cells via modulation of the Wnt/ß-catenin signaling pathway.

LncRNA RHPN1-AS1 Promotes Cell Proliferation, Migration and Invasion Through Targeting miR-7-5p and Activating PI3K/AKT/mTOR Pathway in Hepatocellular Carcinoma.

Hepatocellular carcinoma (HCC) is a severe disease with high mortality in the world. Emerging evidence has suggested that lncRNAs play an important role in cancer progression, including HCC. This study aimed to comprehensively investigate the effect of lncRNA RHPN1 antisense RNA 1 (RHPN1-AS1) on HCC and its underlying molecular mechanism. In this study, we evaluated the expressions of lncRNA RHPN1-AS1 and miR-7-5p by qRT-RCR in both HCC tissue and HCC cells. Our findings showed that lncRNA RHPN1-AS1 was upregulated in HCC tissue and HCC cells, while miR-7-5p was downregulated. LncRNA RHPN1-AS1 expression in HCC patients was closely related to vascular invasion, tumor-node-metastasis (TNM) stage and barcelona clinic liver cancer (BCLC) stage. Furthermore, we quantified cell clone-formation ability, proliferation, migration and invasion of HCCLM3 and MHCC97 H cells using several assays (colony formation assay, 5-Ethynyl-2'-deoxyuridine (EdU) assay and transwell assay, respectively). Functional experiments confirmed that silencing lncRNA RHPN1-AS1 inhibited cell proliferation, migration and invasion in HCCLM3 and MHCC97 H cells. After that, bioinformatics analysis, dual luciferase reporter gene assay, qRT-PCR and western blot were used to investigate the molecular mechanism of lncRNA RHPN1-AS1 on HCC. Mechanistically, the rescue experiments demonstrated that miR-7-5p inhibitor reversed the inhibition effect of silencing lncRNA RHPN1-AS1 on HCCLM3 cells proliferation, migration and invasion. Moreover, silencing lncRNA RHPN1-AS1 also inhibited the activation of PI3K/AKT/mTOR pathway. Taken together our findings demonstrated that lncRNA RHPN1-AS1 could facilitate cell proliferation, migration and invasion via targeting miR-7-5p and activating PI3K/AKT/mTOR pathway in HCC.