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This is an open access article under the terms of the Creative Commons Attribution License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited.

Increasing evidence has suggested that mitochondrial calcium uniporter (MCU) is involved in various types of cancer. However, its functions remain unclear in esophageal cancer. The aim of the present study was to explore its abnormal expression and clinical implications in esophageal cancer. A total of 110 patients with esophageal cancer were enrolled in the study. Western blotting was performed to examine the protein expression levels of MCU in 8 pairs of esophageal cancer and adjacent normal tissues. Using immunochemistry, a total of 110 esophageal cancer specimens were analyzed to identify the association between MCU expression and clinicopathological features of patients with esophageal cancer. Furthermore, immunofluorescence of MCU was performed. Pearson's correlation analysis was performed between MCU and hypoxia inducible factor (HIF)-1α/VEGF/ E-cadherin/Vimentin expression based on western blotting. After KYSE-150 and TE-1 cells were treated with the MCU agonist Spermine and a small interfering RNA against MCU (si-MCU), a series of functional assays were performed, including Cell Counting Kit-8, colony formation and Transwell assays. The results revealed that, compared with in adjacent normal tissues, MCU was highly expressed in esophageal cancer tissues. MCU expression was significantly associated with depth of invasion, lymph node metastasis, TNM stage and distant metastasis. Moreover, MCU was significantly correlated with HIF-1α/VEGF/E-cadherin/Vimentin in esophageal cancer tissues. MCU overexpression promoted VEGF, MMP2, Vimentin and N-cadherin expression, while it inhibited E-cadherin expression in KYSE-150 and TE-1 cells, and opposite results were observed after transfection with si-MCU. Furthermore, MCU overexpression accelerated the proliferation and migration of KYSE-150 and TE-1 cells. Thus, the current findings suggested that high MCU expression may participate in cell proliferation, migration and epithelial-mesenchymal transition in esophageal cancer.

Energy poverty (EP) is a problem that affects developed and developing economies, and its mitigation is of great significance to social welfare. EP affects Latin American countries, and policymakers have recently attempted to address this issue, particularly in the aftermath of the recent economic crisis. It is essential to measure and evaluate EP to implement strategies and policies effectively. Using a panel quantile regression approach, we investigate the heterogeneous impact of green finance, renewable energy (RE), and energy efficiency (EE) on EP for 33 Latin American countries from 2000 to 2018. Furthermore, certain associated control variables are incorporated into our model to avoid an omitted variable bias. According to empirical results, the impact of independent variables on EP is heterogeneous. Specifically, green finance is an essential source of alleviating EP, and it has a significant positive effect across all quantiles, but it is especially strong in the middle quantiles. RE and EE significantly mitigate EP, with the strongest effects occurring at higher quantiles. By including green finance, RE, and EE as the main explanatory determinants of EP, the findings urge policymakers in Latin American countries to design a comprehensive energy conservation policy to minimize the effects of massive EP.