The chemoresistance of colon cancer cells limits the efficacy of chemotherapy. miR-409-3p has been shown to be downregulated in various types of cancer. In the present study, we examined the role of miR-409-3p in colon cancer as well as the effects of miR‑409-3p on the sensitivity of colon cancer cells to oxaliplatin. The expression of miR-409 was significantly downregulated in the human colon cancer cell lines compared with the normal colon epithelial cells. Importantly, the miR-409-3p expression levels were lower in human colon cancer patient samples than in normal colon tissues. Moreover, we observed a negative correlation between the miR‑409-3p levels and resistance to oxaliplatin: the oxaliplatin-resistant colon cancer cells exhibited significantly downregulated miR‑409-3p levels, but higher autophagic activity than the oxaliplatin-sensitive cells. Using bioinformatics analysis, we predicted that miR‑409-3p miRNA binds to the key autophagy gene encoding Beclin-1. Our findings indicated that the overexpression of miR‑409-3p inhibited Beclin-1 expression and autophagic activity by binding to the 3'-untranslated region of Beclin-1 mRNA. In addition, the overexpression of miR‑409-3p enhanced the chemosensitivity of the oxaliplatin-sensitive and oxaliplatin-resistant colon cancer cells. The restoration of Beclin-1 abrogated these effects of miR‑409-3p. In a xenograft model using nude mice, we examined the effects of miR‑409-3p on tumor growth during chemotherapy. miR‑409-3p overexpression sensitized the tumor to chemotherapy, while inhibiting chemotherapy-induced autophagy in a manner dependent on Beclin-1. The findings of our study suggest that miR-409-3p is capable of enhancing the chemosensitivity of colon cancer cells by inhibiting Beclin-1-mediated autophagy.

Introduction Low‐concentration oxygen is an established way for the treatment of chronic obstructive pulmonary disease (COPD) with Type II respiratory failure. Hypercapnia can complicate both COPD exacerbations and stable COPD. Treating with noninvasive ventilation (NIV) can reduce carbon dioxide tension in arterial (PaCO2) in hypercapnic COPD. As an open system, high‐flow nasal cannula oxygen (HFNC) is easy to tolerate and use. More researches are needed to focus on how HFNC is used to treat COPD patients with hypercapnic respiratory failure. Methods The Cochrane Library, Medline, EMBASE, and CINAHL database were retrieved from inception to October 2019. Eligible trials were clinical randomized controlled trials comparing the effects of HFNC and conventional oxygen on hypercapnic COPD patients. Two researchers assessed the quality of each study and extracted the data into RevMan 5.3 independently. The primary outcome was PaCO2 and the secondary outcome was PaO2. Results Four RCTs with 329 patients were included. The research results indicated that PaCO2 in the HFNC group was similar to the conventional oxygen group. No significant difference were observed in PaCO2 (MD −0.98, CI: −2.67 to 0.71, Z = 1.14, p = 0.25) and PaO2 (MD −0.72, CI: −6.99 to 5.55, Z = 0.23, p = 0.82) between the HFNC group and conventional oxygen group. Conclusions Our meta‐analysis showed no difference in PO2 and PCO2 between the HFNC and conventional oxygen. But we should treat this conclusion with caution because the number of studies and participants is small and, there is heterogeneity in the PaO2 and PCO2 measurements between stable and AECOPD.

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Background. High-flow nasal cannula (HFNC) can be used in stable chronic obstructive pulmonary disease (COPD) patients, but the effect of HFNC on clinical outcomes in patients with acute exacerbation of chronic obstructive pulmonary disease (AECOPD) is still uncertain. Methods. We searched electronic literature databases for randomized controlled trials (RCTs) comparing HFNC with noninvasive ventilation (NIV) in hypercapnic patients with AECOPD. The primary endpoint of this meta-analysis was PaCO2, PaO2, and SpO2. The secondary outcomes were the respiratory rate, mortality, complications, and intubation rate. Results. We included 7 RCTs with a total of 481 patients. There were no significant differences on measures of PaCO2 (MD = −0.42, 95%CI −3.60 to 2.75, Z = 0.26, and P  = 0.79), PaO2 (MD = −1.36, 95%CI −4.69 to 1.97, Z = 0.80, and P  = 0.42), and SpO2 (MD = −0.78, 95%CI −1.67 to 0.11, Z = 1.72, P  = 0.08) between the HFNC group and the NIV group. There was no significant difference in measures of the mortality and intubation rate between the HFNC group (OR = 0.72, 95%CI 0.30 to 1.69, Z = 0.76, and P  = 0.44) and the NIV group (OR = 2.38, 95%CI 0.49 to 11.50, Z = 1.08, and P  = 0.28), respectively. But the respiratory rate in the HFNC group was lower than that in the NIV group (MD = −1.13, 95%CI −2.13 to −0.14, Z = 2.23, and P  = 0.03), and fewer complications were found in the HFNC group (OR = 0.26, 95%CI 0.14 to 0.47, Z = 4.46, and P  < 0.00001). Conclusion. NIV was noninferior to HFNC in decreasing PaCO2 and increasing PaO2 and SpO2. Similarly, the mortality and intubation rate was similar among the two groups. The respiratory rate and complications were inferior in the AECOPD group treated with HFNC.