Heat shock protein B7 (HSPB7) inhibits lung adenocarcinoma progression by inhibiting glycolysis.

In the present study, it was aimed to investigate the effects and potential mechanisms of heat shock protein B7 (HSPB7) on lung adenocarcinoma (LUAD). Bioinformatic analysis was performed to explore the association between HSPB7 expression and patients with LUAD. MTT, colony formation, wound healing and Transwell assays were performed to examine the proliferative, migratory and invasive abilities of H1975 and A549 cells. Western blot analysis was conducted to determine the corresponding protein expression. Co­Immunoprecipitation and Chromatin immunoprecipitation assays were carried out to reveal the interaction between HSPB7 and myelodysplastic syndrome 1 and ecotropic viral integration site 1 complex locus (MECOM). In addition, an animal model was conducted by the subcutaneous injection of A549 cells into BALB/c nude mice, and tumor weight and size were measured. HSPB7 was downregulated in LUAD tissues and cells, and its expression level correlated with patient prognosis. Cell functional data revealed that silencing of HSPB7 promoted lung cancer cell proliferation, migration, invasion and epithelial mesenchymal transition (EMT); whereas overexpression of HSPB7 led to the opposite results. Furthermore, bioinformatics analysis showed that HSPB7 inhibited glycolysis. HSPB7 decreased glucose consumption, lactic acid production, and lactate dehydrogenase A, hexokinase 2 and pyruvate kinase muscle isoform 2 protein levels. The results demonstrated that MECOM was a transcription factor of HSPB7. Collectively, these results suggested that HSPB7 is regulated by MECOM, and that HSPB7 attenuates LUAD cell proliferation, migration, invasion and EMT by inhibiting glycolysis.

MiR-29b mimics promotes cell apoptosis of smooth muscle cells via targeting on MMP-2.

The phenotypic transformation and dysfunctions of vascular smooth muscle cells (SMCs) such as abnormality proliferation and apoptosis are key pathological basis of atherosclerosis. The recent study aimed to detect the role of miR-29b in phenotypic transformation of SMCs. In this study, we investigated the expression level of miR-29b and MMP-2 in acute coronary syndrome (ACS) patients, verified whether MMP-2 is the target gene of miR-29b by luciferase reporter gene system, and explored the role of miR-29b in the viability and apoptosis of SMCs. We found that the plasma level of miR-29b was significantly downregulated to 56% of controls (p < 0.01). The plasma level of MMP-2 in health controls was 34.9 ± 6.9 ng/mL, and that it significantly increased to 46.2 ± 13.2 ng/mL in ACS patients. MMP-2 is a target gene of miR-29b. The overexpression of miR-29b significantly downregulated the expression of MMP-2 mRNA and protein. miR-29b mimics inhibited the cell viability of SMCs, and cell apoptosis was significantly enhanced compared with the NC group, especially in the early stage. In the presence of MMP-2 inhibitor SB-3CT, the cell viability and apoptosis of SMC cells were significantly reduced and enhanced, respectively, while the miR-29b -inhibited cell viability and -induced cell apoptosis were not significantly changed. Taken together, miR-29b was downregulated in ACS patients. MiR-29 mimics inhibits cell viability and promotes cell apoptosis via directly targeting on MMP-2, which could be a potentially promising therapy target for cardiovascular diseases.