Emerging evidence has identified the vital role of long noncoding RNAs (lncRNAs) in the development of colorectal cancer. In this study, we aimed to investigate the role of lncRNA gastric carcinoma highly expressed transcript 1 (GHET1) in colorectal cancer. We analyzed the expression of GHET1 in colorectal cancer (CRC) tissues by using ISH. We found that GHET1 expression was significantly increased in the CRC samples compared with adjacent tissues. Furthermore, the cancer tissues had higher GHET1 mRNA levels than their matched adjacent tissues. GHET1 expression was also significantly increased in the CRC cell lines compared with human normal colon epithelial cells. Downregulation of GHET1 mediated by shRNA suppressed the proliferation, cell cycle arrest, migration, and invasion of colorectal cancer cells in vitro. In addition, inhibition of GHET1 reversed the epithelial-mesenchymal transition in colorectal cancer cell lines. Taken together, our results suggest the potential use of GHET1 as a therapeutic target of colorectal cancer.

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Colorectal cancer (CRC) is the third most common cancer with a very poor prognosis predominantly due to its high rate of tumor invasion and migration, and its resistance to anti‑epidermal growth factor receptor (EGFR) therapy. Although CRC has been widely studied, the underlying molecular mechanism remains to be elucidated. MicroRNA (miR)‑133b has been demonstrated to act as a tumor suppressor in several human cancer types by regulating EGFR. However, the detailed involvement of miR‑133b and EGFR in CRC cells remain to be elucidated. The present study used reverse transcription quantitative polymerase chain reaction and characterized the downregulation of the expression levels of miR‑133b in CRC tissues and cell lines. Cell functional assays demonstrated that restored expression of miR‑133b inhibited the growth and invasion of CRC cells. In addition, a luciferase reporter assay revealed that miR‑133b directly targeted EGFR and repressed its expression levels in CRC cells. Additionally, combination treatment with miR‑133b mimics and the monoclonal anti‑EGFR antibody, cetuximab, which is approved and frequently used for treating patients with CRC, exhibited improved inhibitory effects on the growth and invasion of CRC cells compared with treatment with either alone. Taken together, the present study characterized the role of the miR‑133b/EGFR interaction in CRC cells and this suggested the combinational therapy with cetuximab and miR‑133b was positive and may be a potential novel treatment for patients with CRC in the future.

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Airway basal stem cells (BSCs) in the proximal airways are recognized as resident stem cells capable of self-renewing and differentiating to virtually every pseudostratified epithelium cell type under steady-state and after acute injury. In homeostasis, BSCs typically maintain a quiescent state. However, when exposed to acute injuries by either physical insults, chemical damage, or pathogen infection, the remaining BSCs increase their proliferation rate apace within the first 24 h and differentiate to restore lung homeostasis. Given the progenitor property of airway BSCs, it is attractive to research their biological characteristics and how they maintain homeostatic airway structure and respond to injury. In this review, we focus on the roles of BSCs in lung homeostasis and regeneration, detail the research progress in the characteristics of airway BSCs, the cellular and molecular signaling communications involved in BSCs-related airway repair and regeneration, and further discuss the in vitro models for airway BSC propagation and their applications in lung regenerative medicine therapy.

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Green tea (GT) and oolong tea (OLT) are widely consumed beverages, and their preventive and regulatory effects on hypertension have been reported. However, the interventional effects of GT and OLT on hypertension induced by a high-salt diet and its mechanism have not been fully explored. This study evaluated the anti-hypertensive effects of GT and OLT and their underlying mechanisms. The in vivo anti-hypertensive effects of GT and OLT and their capability to prevent hypertension and regulate the intestinal microbiota in Wistar rats fed with a high-salt diet were evaluated. Our results show that GT and OLT supplementations could regulate oxidative stress, inflammation, gene expression, and parameter levels related to blood pressure (BP) and prevent the increase in BP induced by a high-salt diet. Furthermore, both GT and OLT boosted the richness and diversity of intestinal microbiota, increased the abundance of beneficial bacteria and reduced the abundance of harmful bacteria and conditionally pathogenic bacteria, and regulated the intestinal microbial metabolism pathway related to BP. Among them, OLT presented better effects than GT. These findings indicate that GT and OLT can prevent hypertension caused by high-salt diets, which may be due to the regulation of intestinal flora by GT and OLT.