[Corrigendum] Hypoxia­induced internalization of connexin 26 and connexin 43 in pulmonary epithelial cells is involved in the occurrence of non­small cell lung cancer via the P53/MDM2 signaling pathway.

Following the publication of this article, the authors have realized that the corrsesponding author's name was printed incorrectly in the journal: This was mispelled as "Jin Zhou". The corrected name (Jing Zhou) is printed above. The authors regret any inconvenience this has caused, and thank the Editor for allowing them the opportunity to publish a Corrigendum.[the original article was published in International Journal of Oncology 55: 845­859, 2019; DOI: 10.3892/ijo.2019.4867].

Hypoxia­induced internalization of connexin 26 and connexin 43 in pulmonary epithelial cells is involved in the occurrence of non­small cell lung cancer via the P53/MDM2 signaling pathway.

Reports have highlighted an association between connexins (CXs) or gap junction proteins and non­small cell lung cancer (NSCLC). In the present study, it was aimed to elucidate the regulatory mechanism of CX26 and CX43 under hypoxic conditions in NSCLC. Clinical samples were collected for analysis of CX26 and CX43 expression and clinical cancerization followed by quantification of CX26 and CX43 expression. Following the establishment of an in vitro hypoxia model, P53/murine double minute­2 (MDM2) signaling pathway­, proliferation­ and epithelial­mesenchymal transition (EMT)­related genes were quantified to evaluate the influence of CX26 and CX43 on the biological functions of pulmonary epithelial cells in NSCLC. In addition, the proliferation and tumorigenicity of cancer cells were assessed by EdU staining and xenograft tumors, respectively. Decreased expression of CX26 and CX43 was found in cancer tissues compared with surrounding normal tissue. Hypoxia was shown to activate the P53/MDM2 axis and stimulate the downregulation, ubiquitination and degradation of CX26 and CX43, which were translocated from the membrane to the cytoplasm. Low levels of CX26 and CX43 were demonstrated to further promote EMT and the induction of the proliferation and tumorigenicity of cancer cells. These results were reflected by decreased E­cadherin expression and increased N­cadherin expression, along with increased cell migration, promoted cell proliferation ability and elevated relative protein expression of Oct4 and Nanog, and accelerated tumor growth, accompanied by a higher number of metastatic nodes. Taken together, the key observations of the present study demonstrate that the internalization of CX26 and CX43 promoted proliferation, EMT and migration and thus induced NSCLC via aberrant activation of the P53/MDM2 signaling pathway under hypoxic conditions.

MicroRNA-497-5p negatively regulates the proliferation and cisplatin resistance of non-small cell lung cancer cells by targeting YAP1 and TEAD1.

BACKGROUND: MicroRNAs (miRNAs) are crucial regulators in the pathological processes and drug resistance of lung cancer. In this study, we investigated the role of miR-497-5p in modulating the function of non-small cell lung cancer (NSCLC). METHODS: MiR-497-5p expression in lung cancer tissues and cells was evaluated by qRT-PCR. Cell proliferation was evaluated by CCK-8 assay and colony-formation assay. Cell cycle and cell apoptosis were detected by flow cytometry. The effect of miR-497-5p on the expression of Yes-associated protein 1 (YAP1) and TEA domain family member 1 (TEAD1) was analyzed by qRT-PCR, Western blot and luciferase activity assay. RESULTS: The expression of miR-497-5p was significantly downregulated in lung cancer tissues and cells compared with paired normal tissues and cells. Overexpression of miR-497-5p induced growth retardation and apoptosis of A549 lung cancer cells. Mechanistically, YAP1 and TEAD1 were targeted and downregulated by miR-497-5p. Finally, we found that miR-497-5p increased cisplatin chemosensitivity in A549 cells. CONCLUSIONS: MiR-497-5p suppresses cell proliferation and resistance to cisplatin in NSCLC by downregulating the expression of YAP1 and TEAD1.

[Protection of camelliasaponin C against injury of myocardial cells by anoxia/reoxygenation and mechanism thereof].

OBJECTIVE: To investigate the protective effects of camelliasaponin C (CS-C) pretreatment on myocardial cell injury induced by anoxia/reoxygenation. METHODS: Myocardial cells were obtained from neonatal SD rats, cultured for 3 to 4 days, added into the wells of a 24-well plate, and were divided randomly into five groups (8 wells for each group): control group, anoxia/reoxygenation (A/R) group, added with anoxia culture fluid for 3 h and then added with imitation reperfusion fluid for 1 h, anoxia preconditioning (AP) group, undergoing anoxia for 10 min before A/R, CS-C pretreated group, added with CS-C 3.75 x 10(-7) mol/L 1 h before A/R, and glibenclamide (Glib) pretreated group, added with CS-C 3.75 x 10(-7) mol/L and Glib 12 microm 1 h before A/R. Trypan blue exclusion was used to detect the viability of the cardiomyocytes, the contents of lactate dehydrogenase (LDH) in the supernatant of culture medium was measured. Electron microscopy was used to observe the ultrastructure of the cardiomyocytes. RESULTS: The contents of LDH of the A/R group was 57.8 U/L +/- 6.4 U/L, significantly higher than that of the control group (12.3 U/L +/- 1.7 U/L, P < 0.01), and the LDH value of the CS-C group was 39.8 U/L +/- 3.9 U/L, significantly lower than that of the A/R group (P < 0.01), not significantly different from that of the AP group (32.4 U/L +/- 5.2 U/L, P > 0.05), but significantly higher than that of the control group. The cardiomyocyte viability of the A/R group was 51.0% +/- 1.9%, significantly lower than that of the control group (92.0% +/- 2.0%, P < 0.01), the cardiomyocyte viability of the CS-C pretreatment group was 76.4% +/- 3.5%, significantly higher than that of the A/R group (P < 0.01), but not significantly different from that of the AP group (78.0% +/- 2.0%, P > 0.05). The cardiomyocyte ultrastructure of the A/R group was significantly changed, and the changes of cardiomyocyte ultrastructure in the CS-C pretreatment group were significantly attenuated compared with the A/R group. The content of LDH of the Glib group was 55.8 U/L +/- 5.0 U/L, significantly higher than that of the CS-C pretreatment group (P < 0.05), and the cardiomyocyte viability of the Glib group was 54.1% +/- 3.7%, significantly lower than that of the CS-C pretreatment group (P < 0.05), and the damage to the cardiomyocyte ultrastructure in the Glib group was more severe than in the CS-C group. CONCLUSION: The cardioprotective effect of CS-C pretreatment is similar to that of anoxia preconditioning and the effective mechanism would be related to the opening of ATP-sensitive K(+) channel. Glib can abolish the cardioprotective effect of CS-C pretreatment.