[Progress in Gene Polymorphisms Associated With Osteoporosis Susceptibility in Zhuang Ethnic Group in Guangxi].

The purpose of this paper is to systematically summarize the gene polymorphisms associated with osteoporosis(OP)susceptibility in Zhuang ethnic group in Guangxi.These genes mainly encode vitamin D receptor,estrogen receptor,calcitonin receptor,and adiponectin.The genotype and allele distribution frequency were compared between Zhuang ethnic group and other ethnic groups,which can clarify the existing genes and the potential gene polymorphism associated with OP in Zhuang ethnic group.The findings provide a representative solution for the subsequent research on the genes associated with OP susceptibility in ethnic minorities.

The Role of H2-Calponin Antigen in Cancer Metastasis: Presence of Autoantibodies in Liver Cancer Patients.

To investigate the potential of H2-calponin (CNN2) as a serum biomarker for hepatocellular carcinoma (HCC), this study employed the serological analysis of recombinantly expressed cDNA clone (SEREX) technique to identify the presence of CNN2 antibody in the serum of patients with HCC and other tumors. The CNN2 protein was produced through genetic engineering and used as an antigen to determine the positive rate of serum CNN2 autoantibodies via indirect enzyme-linked immunosorbent assay (ELISA). In addition, the mRNA and protein expressions of CNN2 in cells and tissues were evaluated using RT-PCR, in situ RT-PCR, and immunohistochemistry methods. The HCC group exhibited a significantly higher positive rate of anti-CNN2 antibody (54.8%) compared to gastric cancer (6.5%), lung cancer (3.2%), rectal cancer (9.7%), hepatitis (3.2%), liver cirrhosis (3.2%), and normal tissues (3.1%). The positive rates of CNN2 mRNA in HCC with metastasis, non-metastatic HCC, lung cancer, gastric cancer, nasopharyngeal cancer, liver cirrhosis, and hepatitis were 56.67%, 41.67%, 17.5%, 10.0%, 20.0%, 53.13%, and 41.67%, respectively. Meanwhile, the positive rates of CNN2 protein were 63.33%, 37.5%, 17.5%, 27.5%, 45%, 31.25%, and 20.83%, respectively. The down-regulation of CNN2 could inhibit the migration and invasion of liver cancer cells. CNN2 is a newly identified HCC-associated antigen that is implicated in the migration and invasion of liver cancer cells, making it a promising target for liver cancer therapy.

Identification of a Five Immune Term Signature for Prognosis and Therapy Options (Immunotherapy versus Targeted Therapy) for Patients with Hepatocellular Carcinoma.

Background: Immune microenvironment implicated in liver cancer development. Nevertheless, previous studies have not fully investigated the immune microenvironment in liver cancer. Methods: The open-access data used for analysis were obtained from The Cancer Genome Atlas (TCGA-LIHC) and the International Cancer Genome Consortium databases (ICGC-JP and ICGC-FR). R program was employed to analyze all the data statistically. Results: First, the TCGA-LIHC, ICGC-FR, and ICGC-JP cohorts were selected for our analysis, which were merged into a combined cohort. Then, we quantified 53 immune terms in this combined cohort with large populations using the ssGSEA algorithm. Next, a prognostic approach was established based on five immune principles (CORE.SERUM.RESPONSE.UP, angiogenesis, CD8.T.cells, Th2.cells, and B.cells) was established, which showed great prognostic prediction efficiency. Clinical correlation analysis demonstrated that high-risk patients could reveal higher progressive clinical features. Next, to examine the inherent biological variations in high- and low-risk patients, pathway enrichment tests were conducted. DNA repair, E2F targets, G2M checkpoints, HEDGEHOG signaling, mTORC1 signaling, and MYC target were positively correlated with the risk score. Examination of genomic instability revealed that high-risk patients may exhibit a higher tumor mutation burden score. Meanwhile, the risk score showed a strong positive correlation with the tumor stemness index. In addition, the Tumor Immune Dysfunction and Exclusion outcome indicated that high-risk patients could be higher responsive to immunotherapy, whereas low-risk patients may be higher responsive to Erlotinib. Finally, six characteristic genes DEPDC1, DEPDC1B, NGFR, CALCRL, PRR11, and TRIP13 were identified for risk group prediction. Conclusions: In summary, our study identified a signature as a useful tool to indicate prognosis and therapy options for liver cancer patients.

circ_0001588 Induces the Malignant Progression of Hepatocellular Carcinoma by Modulating miR-874/CDK4 Signaling.

Accumulating evidence indicates that circular RNAs (circRNAs) can interact with microRNAs to modulate gene expression in various cancers, including hepatocellular carcinoma (HCC). Although the significant role of circRNAs has been well documented in HCC, the complex mechanisms of circRNAs still need to be elucidated. Our current study is aimed at investigating the function of circ_0001588 in HCC, which was observed to significantly increase in HCC tissues and cells. We demonstrated that the knockdown of circ_0001588 resulted in repressed cell proliferation, migration, and invasion. In vivo studies using a nude mouse model showed that circ_0001588 downregulation reduced tumor size. Moreover, miR-874 was predicted as a target of circ_0001588. Using luciferase binding assays, we proved that circ_0001588 functions as a molecular ceRNA of miR-874 and that CDK4 acts as a downstream target of miR-874 in HCC. It was confirmed that overexpression of miR-874 decreased the proliferation, migration, and invasion triggered by the increase in circ_0001588. In summary, our results indicate that circ_0001588 acts as a ceRNA and promotes HCC progression by targeting the miR-874/CDK4 signaling pathway. Hence, we propose that circ_0001588 may be a promising target for HCC treatment.

MicroRNA-106b-5p inhibits growth and progression of lung adenocarcinoma cells by downregulating IGSF10.

In this study, we investigated the mechanistic role and prognostic significance of IGSF10 in lung adenocarcinoma. Oncomine database analysis showed that IGSF10 expression was significantly reduced in most cancer types, including lung adenocarcinoma (LUAD). In the TCGA-LUAD dataset, IGSF10 expression correlated positively with proportions of tumor-infiltrated B cells, CD4+ T cells, CD8+ T cells, neutrophils, macrophages, and dendritic cells. Kaplan-Meier survival analysis showed that overall survival of patients with low IGSF10 expression was significantly shorter than those with high IGSF10 expression. MiRWalk2.0 database analysis and dual luciferase reporter assays confirmed that miR-106b-5p suppressed IGSF10 expression by binding to its 3'UTR. MiR-106b-5p levels inversely correlated with IGSF10 expression in the TCGA-LUAD dataset. Moreover, inhibition of miR-106b-5p significantly decreased in vitro proliferation, migration, and invasion by LUAD cells, whereas miR-106b-5p overexpression reversed those effects. These results demonstrate that IGSF10 is an independent prognostic factor for LUAD. Furthermore, miR-106b-5p suppressed IGSF10 expression in LUAD tissues by binding to its 3'UTR, which makes IGSF10 and miR-106b-5p potential prognostic biomarkers and therapeutic targets in LUAD patients.

Exogenous regucalcin negatively regulates the progression of cervical adenocarcinoma.

Cervical adenocarcinoma (CA) is a type of cervical cancer, and in previous decades its incidence has steadily increased. The upregulation of regucalcin (RGN) in various tumor cell types inhibits the progression of cancer. To understand the role of RGN in CA, RGN expression in human cervical cancer compared with normal tissues was analyzed using The Cancer Genome Atlas database (TCGA). Subsequently, transfection of lentivirus-mediated RGN into HeLa cells was conducted to study its function in tumor proliferation and metastasis. The expression of RGN and proteins associated with the Wnt/ß-catenin signaling pathway and epithelial-mesenchymal transition (EMT) were determined using reverse transcription-quantitative polymerase chain reaction and western blotting. Cell migration and invasion were evaluated using Transwell assays. Furthermore, cell proliferation, colony formation and cell cycle were assessed using the Cell Counting Kit-8, colony formation assay and flow cytometry, respectively. Lentivirus-mediated RGN effectively upregulated RGN expression, inhibited cell proliferation, retarded cellular invasion and promoted cell cycle arrest at the G2/M phase in HeLa cells. In addition, the expression levels of ß-catenin, p-glycogen synthase kinase (GSK)-3ß, matrix metalloproteinase (MMP)-3, MMP-7 and MMP-9 were effectively decreased, whilst those of E-cadherin and GSK-3ß were increased. The results suggest that RGN may be an inhibitory factor in tumorigenesis, and its mechanism of inhibiting tumor proliferation and metastasis may be associated with Wnt/ß-catenin signaling and EMT.