In silico identification and in vitro evaluation of MRPS30-DT lncRNA and MRPS30 gene expression in breast cancer.

BACKGROUND: It has been reported that long non-coding RNAs (lncRNAs) can play important roles in a variety of biological processes and cancer regulatory networks, including breast cancer. AIMS: This study aimed to identify a novel upregulated lncRNA in breast cancer and its associated gene using bioinformatics analysis, and then evaluate their potential roles in breast cancer. METHODS AND RESULTS: Extensive in silico studies were performed using various bioinformatics databases and tools to identify a potential upregulated breast cancer-associated lncRNA and its co-expressed gene, and to predict their potential roles, functions, and interactions. The expression level of MRPS30-DT lncRNA and MRPS30 was assessed in both BC tissues and cell lines using qRT-PCR technology. MRPS30-DT lncRNA and MRPS30 were selected as target genes using bioinformatics analysis. We found that MRPS30-DT and MRPS30 were significantly overexpressed in BC tissues compared with normal tissues. Also, MRPS30 showed upregulation in all three BC cell lines compared with HDF. On the other hand, MRPS30-DT significantly increased in MDA-MB-231 compared with HDF. While the expression of MRPS30-DT was significantly dropped in the resistance cell line MCF/MX compared to HDF and MCF7. Moreover, bioinformatics analysis suggested that MRPS30-DT and MRPS30 may play a potential role in BC through their involvement in some cancer signaling pathways and processes, as well as through their interaction with TFs, genes, miRNAs, and proteins related to carcinogenesis. CONCLUSIONS: Overall, our findings showed the dysregulation of MRPS30-DT lncRNA and MRPS30 may provide clues for exploring new therapeutic targets or molecular biomarkers in BC.

Genetic polymorphisms of MRPS30-DT and NINJ2 may influence lung cancer risk.

Lung cancer is one of the malignant tumors, and genetic background is a risk factor in lung cancer that cannot be neglected. In this study, we aimed to find out the effect of MRPS30-DT and NINJ2 variants on lung cancer risk. In this study, the seven selected single-nucleotide polymorphisms (SNPs) of MRPS30-DT and NINJ2 were genotyped in 509 lung cancer patients and 501 healthy controls based on the Agena MassARRAY platform. Odds ratios and 95% confidence intervals were calculated by logistic regression analysis to evaluate association between gene polymorphisms and lung cancer risk. False-positive report probability was also used to assess false-positive results. Furthermore, the interaction between SNPs was analyzed by multifactor dimensionality reduction to predict lung cancer risk. We identified the genotype TA of rs16901963 (T < A) in MRPS30-DT as a protective factor against lung cancer, while rs16901963-TT was significantly associated with an increased risk of lung cancer. We also revealed that the effect of MRPS30-DT and NINJ2 variants on the risk of lung cancer was dependent on age, gender, smoking, and drinking status. In conclusion, this study first proved that MRPS30-DT and NINJ2 variants played important roles in affecting the susceptibility to lung cancer.

The contribution of the LOC105371267 and MRPS30-DT genetic polymorphisms to IgA nephropathy in the Chinese Han population.

BACKGROUND: IgA nephropathy (IgAN) is the most common primary glomerulonephritis worldwide. Genetic factors are reported to play an essential role in IgAN progression. This study was designed to investigate the association between LOC105371267 and MRPS30-DT and IgAN risk among the Chinese Han population. METHODS: Six SNPs were genotyped. A logistic regression model was used to calculate the effects of the candidate SNPs on IgAN. The SNP-SNP interaction was analyzed using multifactor dimensionality reduction. RESULTS: We observed that only LOC105371267 had a relationship with IgAN. The results indicated an association between the genotype "CC" and a decreased IgAN risk (OR=0.44, P=0.014). The stratification analysis of the patients over 35 years old showed that rs3931698 contributes to IgAN susceptibility in the "GT" genotype (OR=1.78, P=0.038), while rs8044565 showed a significantly decreased risk-effect with IgAN ("T", OR=0.59, P=0.006; "CC", OR=0.15, P=0.015; "CC-CT", OR=0.59, P=0.023; Log-additive, OR=0.56, P=0.005). rs8044565 was correlated with a decreased susceptibility of IgAN in males ("CC", OR=0.27, P=0.006) and in patients with a Lee's grade ≥III ("CC", OR=0.46, P=0.046). We found rs8044565 is related to systolic blood pressure and urinary casts and rs3852740 has a relationship with the serum C3 and hemoglobin levels (P<0.05). CONCLUSION: The present study demonstrated that the SNPs in long non-coding RNAs might be related to IgAN.

MRPS30-DT Knockdown Inhibits Breast Cancer Progression by Targeting Jab1/Cops5.

Longnoncoding RNAs (lncRNAs) are significantly correlated with cancer pathogenesis, development, and metastasis. Microarray analysis showed that lncRNA MRPS30-DT is overexpressed in breast carcinoma; however, the function of MRPS30-DT in breast cancer tumorigenesis remains unclear. In situ hybridization and immunohistochemical analysis were used to evaluate the expression levels of MRPS30-DT and Jab1 in clinical samples of breast carcinoma and their relation to survival outcome. qRT-PCR was used to measure MRPS30-DT and Jab1 mRNA expressions. Protein levels were detected using Western blot. Cell proliferation and invasion ability were evaluated via 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT), colony formation, and transwell assays. MRPS30-DT was knocked down in breast cancer cells to investigate its potential functional roles in cell growth and metastasis in vitro and in vivo. We found that MRPS30-DT was upregulated in breast cancer specimens and was accompanied by high Jab1 expression compared with that of paired para-carcinoma tissues. Knocking down MRPS30-DT significantly inhibited cancer cell proliferation and invasion and induced apoptosis in breast cancer cells. Similarly, knocking down MRPS30-DT in MDA-MB-231 cells significantly suppressed tumor growth. Furthermore, knocking down MRPS30-DT markedly reduced Jab1 expression in breast cancer cells and murine carcinoma. Statistical analyses suggested that high MRPS30-DT or Jab1 levels in breast cancer patients were positively correlated with poor prognoses. These data indicate the possible mechanisms of MRPS30-DT and Jab1 in breast cancer; thus, MRPS30-DT and Jab1 may be novel prognostic biomarkers and potential therapeutic targets for breast cancer treatment.