Kutkoside-an iridoid glycoside, exerts anti-proliferative effects in drug-resistant human oral carcinoma cells by targeting PI3K/AKT signalling pathway, inducing apoptosis and suppressing cell migration and invasion.

The Editors of JBUON issue an Expression of Concern to ' Kutkoside-an iridoid glycoside, exerts anti-proliferative effects in drug-resistant human oral carcinoma cells by targeting PI3K/AKT signalling pathway, inducing apoptosis and suppressing cell migration and invasion', by Jun-Chi Hou, Xiao-Nan Xu, JBUON 2020;25(1):338-343; PMID: 32277652. Following the publication of the above article, readers drew to our attention that part of the data was possibly unreliable. We sent emails to the authors with a request to provide the raw data to prove the originality, but received no reply. Therefore, as we continue to work through the issues raised, we advise readers to interpret the information presented in the article with due caution. We thank the readers for bringing this matter to our attention. We apologize for any inconvenience it may cause.

Kutkoside-an iridoid glycoside, exerts anti-proliferative effects in drug-resistant human oral carcinoma cells by targeting PI3K/AKT signalling pathway, inducing apoptosis and suppressing cell migration and invasion.

PURPOSE: The main purpose of the current research work was to investigate the anticancer potential of Kutkoside -a naturally occurring iridoid glycoside, against drug-resistant human oral carcinoma cells along with evaluating its effects on PI3K/AKT signalling pathway, cellular apoptosis, cell migration and cell invasion. METHODS: Cell viability was assessed by using MTT colorimetric assay, while effects on cellular apoptosis were evaluated by acridine orange (AO)/ethidium bromide (EB) as well as by using flow cytometry employing annexin V-FITC. Effects on cell migration and cell invasion were evaluated by in vitro wound healing assay and transwell Matrigel assay. Effects on PI3K/AKT signalling pathway were evaluated by western blot method. RESULTS: Kutkoside led to significant and dose-dependent inhibition of HSC-2 human oral cancer cells using doses of 0, 1.25, 2.5, 5, 10, 20, 40, 80 and 160 µM. Fluorescence microscopy revealed that on increasing the dose of kutkoside, the number of both apoptotic and necrotic cells increased, showing that Kutkoside induces apoptotic cell death in HSC-2 oral cancer cell line in dose-dependent manner. Flow cytometry indicated that the percentage of apoptotic cells at different dose exposures of Kutkoside, namely 0, 8, 16 and 32 µM was 4.9%, 12.18%, 22.18% and 34.10%, respectively. Kutkoside treatment also led to cell migration inhibition and cell invasion inhibition. This molecule upregulated the expression of AKT and PI3K, simultaneously downregulating the expressions of p-AKT and p-PI3K in a dose-dependent manner. CONCLUSION: Kutkoside shows potential anticancer and pro-apoptotic effects in HSC-2 oral carcinoma cells and as such may be developed as a possible anticancer agent provided further studies are performed.

[Expression of CXC chemokine ligand 16 and chemokine receptor 6 in periodontal tissues of patients with moderately severe periodontitis].

PURPOSE: To investigate the expression and localization of CXCLl6 and its receptor CXCR6 in gingival tissues of patients with chronic periodontitis and analyze the roles in the occurrence and development of periodontitis. METHODS: Gingival tissues with moderately severe periodontitis were collected from 39 patients treated in People's Hospital of Liaoning Province. Forty persons with healthy gingiva were used as control. The age of the enrolled subjects ranged from 35 to 74 years old. Immunohistochemical technique was applied to detect the expression and localization of CXCLl6 and CXCR6 protein gingival tissues of all subjects. The data was analyzed with SPSS 15.0 software package. RESULTS: Compared with normal group, the expression of CXCLl6 and CXCR6 were significantly up-regulated in patients with periodontitis (P<0.05). There was a positive relationship between the protein expression of CXCLl6 and CXCR6 in gingival tissues of patients with periodontitis (r=0.580, P<0.05). CONCLUSIONS: CXCLl6 and CXCR6 may be involved in the development of chronic periodontitis. The expression of CXCLl6 and CXCR6 may work coordinately to promote the development of chronic periodontitis.