Long non­coding RNA LINC00312 regulates breast cancer progression through the miR­9/CDH1 axis.

Long non­coding RNAs (lncRNAs) are important mediators of the initiation and progression of tumors, including breast cancer (BC). The exact role of long intergenic non­coding RNA 00312 (LINC00312) in BC and its mechanism of action have not been reported to date. In the present study, LINC00312 was found to be downregulated in human BC tissues and cell lines by RT­qPCR. The findings of a functional study indicated that overexpression of LINC00312 suppressed the proliferation, colony forming ability, migration and invasiveness of BC cell lines. Mechanistically, LINC00312 was found to induce suppression of cell migration and invasion by directly binding to miR­9. Overexpression of LINC00312 increased the expression of cadherin 1 (CDH1), a direct target of miR­9, and decreased the expression of vimentin (VIM), a major cytoskeletal component of mesenchymal cells as determined by western blot analysis. miR­9 partly abrogated the upregulation of CDH1 and downregulation of VIM induced by LINC00312. Taken together, the results of the present study indicate a role for the LINC00312/miR­9/CDH1 axis in the progression of BC, and suggest a novel lncRNA­based diagnostic biomarker or therapeutic target for BC.

[The application of multiplex ligation-dependent probe amplification technology in diagnosis and prenatal diagnosis of α-thalassemia].

OBJECTIVE: To investigate the multiplex ligation-dependent probe amplification (MLPA) technology in the detection of gene deletion and prenatal diagnosis of α-thalassaemia. METHODS: Phenotypes were analyzed by whole blood cell counting and hemoglobin component detection of peripheral blood samples from the subjects. The gene deletions and point mutations of α- thalassaemia were detected with regular gap-PCR and reverse dot blot (RDB) method. At last, the MLPA method was applied for detection of α-globin gene deletion. All the prenatal diagnosis samples were detected with both gap-PCR and MLPA method. RESULTS: α-thalassaemia phenotype was found in 75 samples from 1256 (628 couples) peripheral blood samples for pre-pregnancy or prenatal thalassemia gene screening. Among them, 71 samples carrying α-gene mutations and consistent with phenotypes were detected by routine methods. In the other 3 samples with no α-gene mutations detected and 1 sample with HbH phenotype but genotype of ï¹£α(4.2)/αα were analyzed by MLPA and found each one samples of whole α-globin gene cluster deletion, respectively. Seventeen high risk couples were screened. Among the 17 prenatal diagnosis samples, 2 villus samples contaminated by exogenous DNA were confirmed by MLPA method. CONCLUSION: MLPA is an effective complement for α-thalassaemia gene deletion detection. The molecular diagnosis strategy and process of gap-PCR combined with MLPA for α- thalassaemia gene deletion detection can prevent the missing of gene deletion, and false-positive or false-negative misdiagnosis of α-thalassaemia in prenatal diagnosis.