Erratum: [Corrigendum] miR­137 suppresses proliferation, migration and invasion of colon cancer cell lines by targeting TCF4.

[This corrects the article DOI: 10.3892/ol.2018.8364.].

Baicalin inhibits inflammation and apoptosis of interstitial cells of Cajal by targeting the NF-κB-mediated AMPK/Erk/Akt pathway in an ulcerative colitis rat model.

BACKGROUND AND AIMS: An ulcerative colitis rat model was established with baicalin as the treatment. MATERIALS AND METHODS: Quantitative real-time polymerase chain reaction (QRT-PCR) and Western blot analysis were used to determine inflammatory factor expression in interstitial cells of Cajal. RESULTS: Baicalin treatment reduced the ulcerative colitis symptoms, such as bloody diarrhea, reduction in body weight, and vomiting. Baicalin treatment decreased the serum levels of tumor necrosis factor α (TNFα), interleukin (IL)-1ß, and IL-17A compared to the phosphate buffer saline (PBS) control group. Baicalin treatment protected the interstitial cells of Cajal against oxidative stress injury via improvements in superoxide dismutase (SOD) activity, modified disease activity index (mDAI), reactive oxygen species (ROS) production, catalase (CAT), glutathione (GSH), and nitric oxide (NO) level in the serum and interstitial cells of Cajal. Baicalin treatment decreased apoptosis of interstitial cells of Cajal. Baicalin treatment decreased the nuclear factor Kappa B (NF-κB)/ Adenosine 5'-monophosphate (AMP)-activated protein kinase (AMPK)/ extracellular regulated kinase (Erk) / protein kinase B (Akt) signal pathway in interstitial cells of Cajal and NF-κB overexpression abrogated the decreased baicalin-induced inflammation and apoptosis of interstitial cells of Cajal induced. CONCLUSION: Baicalin treatment improved ulcerative colitis symptoms and decreased inflammation and apoptosis of interstitial cells of Cajal. Baicalin treatment inhibited inflammation and apoptosis of interstitial cells of Cajal by targeting the NF-κB pathway in an ulcerative colitis rat model, which may serve as a potential agent for the treatment of ulcerative colitis.

Long non-coding RNA NKILA serves as a biomarker in the early diagnosis and prognosis of patients with colorectal cancer.

Colorectal cancer (CRC) is one of the leading causes of cancer-associated mortality worldwide. The prognosis of patients with CRC at an advanced stage is poor. Biomarkers currently used in clinical practice, including carcinoembryonic antigen (CEA) and cancer antigen (CA) 19-9, lack sufficient sensitivity and specificity for early diagnosis and prediction, therefore there remains a requirement to improve the prognosis of patients with CRC. Long non-coding RNAs (lncRNAs) have been revealed to serve fundamental roles in various pathophysiological processes, including cancer initiation and progression. The present study investigated the expression and clinical significance of the lncRNA nuclear factor-κB interacting long non-coding RNA (NKILA) in CRC. It was identified that NKILA was downregulated in six CRC cell lines and tissues (n=173). Low NKILA expression was significantly associated with a poor differentiation grade, larger tumor size and advanced Tumor-Node-Metastases stages. Further statistical analyses revealed that low NKILA expression predicted poor overall survival (OS) rate and progression-free survival (PFS) rate. In addition, low NKILA expression was determined as an independent risk factor for poor OS and PFS. Furthermore, NKILA exhibited a relatively high sensitivity and specificity compared with CEA and CA19-9 in the early diagnosis of CRC. The serum level of NKILA was positively correlated with the level in tissues. In addition, a decreased NKILA level in serum was revealed to be partially restored post-operatively. In conclusion, low NKILA expression has been demonstrated to accelerate CRC progression and NKILA may be a potential novel biomarker in early diagnosis and prognosis of patients with CRC.

Expression of a Novel Long Noncoding RNA (lncRNA), GASL1, is Downregulated in Patients with Intracranial Aneurysms and Regulates the Proliferation of Vascular Smooth Muscle Cells In Vitro.

BACKGROUND Preliminary microarray data in our laboratory indicated that the novel long noncoding RNA (lncRNA), GASL1, was downregulated in patients with intracranial aneurysms. This study aimed to investigate the expression of lncRNA GASL1 in patients with intracranial aneurysms and its role in the regulation of vascular smooth muscle cell (VSMC) proliferation by transforming growth factor-ß1 (TGF-ß1). MATERIAL AND METHODS The study included 68 patients with unruptured intracranial aneurysms and 56 healthy volunteers. In both groups, serum levels of TGF-ß1 were measured using an enzyme-linked immunoassay (ELISA) and Western blot. Human VSMCs in vitro underwent lncRNA GASL1 overexpression using the insertion of an EcoRI-EcoRI fragment into the pIRSE2 vector. Cell viability and proliferation were measured by a cell counting kit-8 (CCK-8) assay. RNA extraction and quantitative real-time polymerase chain reaction (qRT-PCR) determined GASL1 expression. RESULTS ROC curve analysis showed that downregulation of GASL1 effectively distinguished patients with intracranial aneurysm from healthy controls. Blood GASL1 and TGF-ß1 were negatively correlated in patients with intracranial aneurysm but not in healthy people. GASL1 overexpression promoted proliferation of human vascular smooth muscle cells (VSMCs) and downregulated TGF-ß1 expression, while exogenous TGF-ß1 reduced VSMCs proliferation but showed no effects on GASL1 expression.  CONCLUSIONS Expression of the novel lncRNA, GASL1, was downregulated in patients with intracranial aneurysms and regulated the proliferation of VSMCs in vitro by targeting TGF-ß1.

miR-137 suppresses proliferation, migration and invasion of colon cancer cell lines by targeting TCF4.

Colorectal cancer is cancer of the colon or rectum and is the third most prevalent form of cancer. Currently, there are several shortcomings in the prognosis and early detection of colon cancer. The present study aims to address questions pertaining to the role of microRNA (miR)-137 in colon cancer progression and the mode of regulation. The endogenous and over-expressed levels of miR-137 in three colon cancer cell lines were assessed by reverse transcription-quantitative polymerase chain reaction (RT-qPCR). The MTT assay was used to assess cell proliferation. Cell migration and invasion assays were assessed using Transwell apparatus and Matrigel invasion chambers. The potential targets of miR-150 were predicted using TargetScan software, and one of the best scoring targets, transcription factor 4 (TCF4), was experimentally validated using western blot analysis and RT-qPCR. It was found that that miR-137 is expressed at extremely low levels in COLO205, HCT116 and SW480 cell lines. Cell proliferation, migration and invasion were inhibited subsequent to transfection of the colon cancer cell lines with miR-137. Using bioinformatics analysis, the best scoring putative targets were identified. One such target, TCF4, was experimentally validated, and it was shown that overexpression of miR-137 suppresses TCF4 in all three colon cancer cell lines. In conclusion, it was shown that miR-137 inhibits cell proliferation, migration and invasion in colon cancer cell lines by negatively regulating the expression of TCF4.

ANTI-ULCEROGENIC EFFICACY AND MECHANISMS OF EDIBLE AND NATURAL INGREDIENTS IN NSAID-INDUCED ANIMAL MODELS.

BACKGROUND: Nonsteroidal anti-inflammatory drugs (NSAIDs) are a class of the most commonly used medicines and proven to be effective for certain disorders. Some people use NSAIDs on daily basis for preventive purpose. But a variety of severe side effects can be induced by NSAIDs. Studies have shown that edible natural ingredients exhibit preventive benefit of gastric ulcer. This paper reviews the efficacy and safety of edible natural ingredients in preventing the development of gastric ulcer induced by NSAIDs in animal models. METHODS: A systematic literature search was conducted on PubMed, using the terms "herbal medicines" and "gastric ulcer", "herbal medicines" and "peptic ulcer", "food" and "peptic ulcer", "food" and "gastric ulcer", "natural ingredient" and "peptic ulcer", "natural ingredient" and "gastric ulcer", "alternative medicine" and "peptic ulcer", "alternative medicine" and "gastric ulcer", "complementary medicine" and "peptic ulcer", "complementary medicine" and "gastric ulcer" in papers published in English between January 1, 1960 and January 31, 2016, resulting in a total of 6146 articles containing these terms. After exclusion of studies not related prevention, not in NSAID model or using non-edible natural ingredients, 54 articles were included in this review. RESULTS: Numerous studies have demonstrated that edible natural ingredients exhibit antiulcerogenic benefit in NSAID-induced animal models. The mechanisms by which edible, ingredient-induced anti-ulcerogenic effects include stimulation of mucous cell proliferation, antioxidation, inhibition of gastric acid secretion, as well as inhibition of H (+), K (+)- ATPase activities. Utilization of edible, natural ingredients could be a safe, valuable alternative to prevent the development of NSAID-induced gastric ulcer, particularly for the subjects who are long-term users of NSAIDs.

Evaluation of 6-chloro-N-[3,4-disubstituted-1,3-thiazol-2(3H)-ylidene]-1,3-benzothiazol-2-amine Using Drug Design Concept for Their Targeted Activity Against Colon Cancer Cell Lines HCT-116, HCT15, and HT29.

BACKGROUND Colorectal adenocarcinoma is the second leading cause of cancer-related death in the world. The stage of the disease is related to the survival of the patient, and in early phases surgery is the main modality of treatment. The main aim of modern medicinal chemistry is to synthesize small molecules via drug designing, especially by targeting tumor cells. MATERIAL AND METHODS A new series of 19 compounds containing benzothiazole and thiazole were designed. Molecular docking studies were performed on the designed series of molecules. Compounds showing good binding affinity towards the EGFR receptor were selected for synthetic studies. Characterization of the synthesized compounds was done by FTIR, 1HNMR, Mass and C, H, N, analysis. RESULTS The anticancer evaluation of the synthesized compounds was done at NIC, USA at a single dose against colon cancer cell lines HCT 116, HCT15, and HC 29. The active compounds were further evaluated for the 5-dose testing. Compounds were designed by using docking analysis. To ascertain the interaction of EGFR tyrosine kinase binding, energy calculation was used. CONCLUSIONS The results of the present study indicate that the designed compounds show good activity against colon cancer cell lines, which may be further studied to design new potential molecules.

Efficacy and safety of herbal medicines in treating gastric ulcer: a review.

Gastric ulcer is a common disorder of the digestive system. Current therapeutic regimens largely rely on Western medicine. However, numerous studies have demonstrated that herbal medicines can effectively treat gastric ulcer in humans and various animal models via divergent mechanisms. This review updates the efficacy and safety of herbal medicines in treating gastric ulcer, and the mechanisms of their action in humans and animal models. Studies have demonstrated that the efficacy of herbal medicines is comparable or superior to that of drugs such as omeprazole or cimetidine in humans and animal models, and herbal medicines display fewer adverse effects. The mechanisms by which herbal medicines benefit gastric ulcer include stimulation of mucous cell proliferation, anti-oxidation, and inhibition of gastric acid secretion and H(+)/K(+)-ATPase activity. Some herbal medicines also exhibit antimicrobial properties. Utilization of herbal medicines could be a valuable alternative to treat gastric ulcer in humans effectively, with few adverse effects.

Comparison of publication trends in dermatology among Japan, South Korea and Mainland China.

BACKGROUND: We previously showed that the number of publications in dermatology is increasing year by year, and positively correlates with improved economic conditions in mainland China, a still developing Asian country. However, the characteristics of publications in dermatology departments in more developed Asian countries such as Japan and South Korea are unknown. METHODS: In the present study, publications from 2003 through 2012 in dermatology in Japan, South Korea and mainland China were characterized. All data were obtained from http://www.pubmed.com. RESULTS: Dermatology departments in Japan published 4,094 papers, while mainland China and South Korea published 1528 and 1,758 articles, respectively. 48% of articles from dermatology in Japan were original research and 36% were case reports; The number of publications in Japan remained stable over time, but the overall impact factors per paper increased linearly over the last 10 year period (p < 0.05). In mainland China, 67% of articles from dermatology were original research, while 19% were case reports; The number of publications and their impact factors per paper increased markedly. In South Korea, 65% of articles from dermatology were original research and 20% were case reports. The impact factors per paper remained unchanged, despite of the fact that the number of publications increased over the last 10 year period (r2 = 0.6820, p = 0.0032). Only mainland China showed a positive correlation of the number of publications with gross domestic product per capita during this study period. CONCLUSIONS: These results suggest that the total number of publications in dermatology correlates with economic conditions only in developing country, but not in more developed countries in Asia. The extent of economic development could determine both the publication quantity and quality.