Tao Huang

Guangdong Ocean University

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Guangjian Jiang

Beth Israel Deaconess Medical Center

Chunping Zou

Wuhan University of Science and Technology

Weihua Gong

Zhengzhou Children's Hospital

Xiucheng Li

Henan University of Science and Technology

Robin F. Krimm

University of Louisville

Wei Chen

Chinese Academy of Medical Sciences & Peking Union Medical College

Hong You

Beijing Friendship Hospital

Xuzhen Yan

Beijing Friendship Hospital

Aiting Yang

Beijing Friendship Hospital

Jidong Jia

Beijing Friendship Hospital

Cooperative Institutions

China Medical University

Huazhong University of Science and Technology

Capital Medical University

Chinese Academy of Sciences

Sun Yat-sen University

National Clinical Research Center for Digestive Diseases

Chinese Academy of Medical Sciences & Peking Union Medical College

Central South University

Beijing Friendship Hospital

First Hospital of China Medical University

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Exosomal microRNA-155 as a biomarker for hepatic fibrosis diagnosis and progression

Annals of Translational Medicine (2021)

Lianjie Niu Yamin Zhang Tao Huang Xianfu Sun Suxia Luo

Pathological examination of liver biopsies remains the gold standard for evaluating the stage of hepatic fibrosis, which are a number of disadvantages associated with biopsy. The aim of the present study was to investigate the potential of exosomal microRNA (miR)-155 as a non-invasive biomarker for the diagnosis and progression of hepatic fibrosis.Exosomal miR-155 quantity was analyzed by sampling serum exosomes of patients with hepatic fibrosis and a hepatic fibrosis rat model. A total of 94 patients were divided into three groups based on Child-Pugh rating. Additionally, 30 patients with primary liver fibrosis who underwent liver transplantation were divided into the low miR-155 expression group and the high expression group; 56 rats were divided into 7 groups (n=8, 0, 2, 4, 6, 8, 10, and 12 weeks). Rats in every group were intravenously injected with CCl4 (3% vol/vol in olive oil; 0.3 mL/100 g body weight) twice weekly to produce different degrees of liver necrosis and liver fibrosis.Exosomal miR-155 was found to be closely associated with the progression of cirrhosis and clinical prognostic indicators of cirrhosis. Exosomal miR-155 gradually increased with the severity of hepatic necrosis and fibrosis.The findings of the present study indicate that exosomal miR-155 can act as a non-invasive biomarker for the diagnosis and progression of hepatic fibrosis.

Hepatic fibrosis

Hepatic stellate cell

10.21037/atm-20-7787

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Citations (19)

[Minimally invasive surgery for knee osteoarthritis].

PubMed (2023)

Pengfei Xing Junsong Qu Tao Huang

Knee surgery

Invasive surgery

10.12200/j.issn.1003-0034.2023.06.001

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Identification of Max binding protein as a novel binding protein of Nck1 and characterization of its role in inhibiting human liver cancer SK-HEP-1 cells.

PubMed (2012)

Qi Zhou Tao Huang Yafeng Wang Kun-sun Zhang Dong Chen

The tendency of tumor cells to disperse throughout the liver is a distinct feature of hepatocellular carcinoma (HCC). Nck family adaptor proteins function to regulate actin cytoskeletal reorganization that leads to cell motility. We previously found that Max binding protein (MNT) was differentially expressed in HCC, and interacted with Nck1 by 2-DE. MNT is a protein member of the Myc/Max/Mad network which plays roles in cell proliferation, differentiation, and death. We investigated the effects of MNT on migration of human liver cancer SK-HEP-1 cells to study the migration regulatory role of MNT in HCC cells.Interaction between MNT and Nck1 was further validated in hepatoma cells by GST-pull down assay and immunoprecipitation. siRNAs specific to MNT (MNT siRNA) were used to knockdown MNT expression. Western blotting, transwell assay were used to determine the migration potential of cells.Interaction between MNT and Nck1 was validated in hepatoma cells. MNT knockdown promoted the migration of human liver cancer SK-HEP-1 cells (P < 0.01).The results suggest that MNT, via interaction with Nck1, inhibits hepatoma cell migration.

Liver Cancer

Immunoprecipitation

Liver cell

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Citations (4)

Correction: Corrigendum: Overexpression of miRNA-497 inhibits tumor angiogenesis by targeting VEGFR2

Scientific Reports (2016)

Yingfeng Tu Li Liu Dongliang Zhao Youbin Liu Xiaowei Ma

Scientific Reports 5: Article number: 13827; published online: 08 September 2015; updated: 16 February 2016. In this Article, Figure 4 is incorrect. The correct Figure 4 appears below as Figure 1.

10.1038/srep21221

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Long non-coding RNA NEAT1 promotes proliferation, migration and invasion of human osteosarcoma cells

International Journal of Medical Sciences (2018)

Pengcheng Li Rui Huang Tao Huang Shuo Cheng Yao Chen

Aim: Long non-coding RNAs (LncRNAs) have been identified to play a crucial role in tumorigenesis and the progression of many types of tumors.However, the clinical significance and biological function of lncRNA nuclear-enriched abundant transcript 1(NEAT1) in human osteosarcoma remains unknown.Here, we investigated the role of NEAT1 in human osteosarcoma cell lines and clinical tumor samples.Methods: In this study, expression of NEAT1 was analyzed in 19 osteosarcoma tissues and paired adjacent non-tumor tissues by using quantitative real-time PCR.Additionally, knockdown of NEAT1 expression using Lentivirus-mediated siRNA was performed in order to explore the biological function of NEAT1 on osteosarcoma cell proliferation and metastasis through MTT, colony formation assay and transwell assay.Results: NEAT1 was over-expressed in osteosarcoma tissues compared with adjacent non-tumor tissues.In addition, knockdown of NEAT1 expression could suppress cell proliferation, migration and invasion in vitro.Conclusion: LncRNA NEAT1 was up-regulated in osteosarcoma tissue, promoting proliferation and metastasis of osteosarcoma cells.These findings indicate the role of this substance, as a growth regulator in osteosarcoma, and thus it may serve as a novel biomarker, and drug target for developing osteosarcoma therapies.

MTT assay

Gentamicin protection assay

10.7150/ijms.25662

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Citations (27)

[The influence of the recombinant lentiviral vectors encoding Hyper-IL-6 on the proliferation of human hepatic cell].

PubMed (2009)

Sun Wen-jing Bo Qin Tao Huang Ailong Huang

To investigate the effect of Hyper-IL-6 on the proliferation of L-02 cells.The recombinant lentiviral vectors encoding Hyper-IL-6 (FIV-Hyper-IL-6), IL-6 (FIV-IL-6) and the lentiviral (FIV) were prepared using the FIV-based lentiviral vectors and the packaging system. The titer of FIV-Hyper-IL-6, FIV-IL-6 and FIV was tested with puromycin. L-02 cells were infected with FIV-Hyper-IL-6, FIV-IL-6, FIV, or mock-infected. The growth rate of L02 cells was analyzed with MTT at different time points after infection. The changes of Haptoglobin in L-02 cells were analyzed with RT-PCR.FIV-Hyper-IL-6, FIV-IL-6 and FIV were successfully constructed, and the titer was 107 pfu/ml. 48 hours after infection, the absorbance of the cells infected with FIV-Hyper-IL-6 was 0.6267+/-0.0256, and the absorbances of FIV-IL-6 infected cells, FIV infected cells and mock-infected cells were 0.5563+/-0.0112, 0.5040+/-0.0078 and 0.4790+/-0.0201, respectively. There were significant differences between the FIV-Hyper-IL-6 group and the other groups (F = 41.09, P less than 0.01). The ratio of the absorbance between haptoglobin mRNA and beta-actin was 0.7030+/-0.0106, 0.3355+/-0.0093, 0.1145+/-0.0076 and 0.1143+/-0.0153, respectively, in FIV-Hyper-IL-6 infected cells, FIV-IL-6 infected cells, FIV infected cells and mock-infected cells. There were significant differences between the FIV-Hyper-IL-6 group and the others (q = 57.5007, P less than 0.01).Compared with IL-6, Hyper-IL-6 is more potent to stimulate proliferation and induce the expression of Haptoglobin in L-02 cells.

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MicroRNA miR-331-3p suppresses osteosarcoma progression via the Bcl-2/Bax and Wnt/β-Catenin signaling pathways and the epithelial-mesenchymal transition by targeting N-acetylglucosaminyltransferase I (MGAT1)

Bioengineered (2022)

Wen Bi Mengyue Yang Pengfei Xing Tao Huang

Osteosarcoma (OS) is a high-grade malignant disease that is a prevalent primary malignant sarcoma of the bone. The purpose of this investigation was to therefore elucidate the association between miR-331-3p and OS development and to identify a potential underlying mechanism. Key genes involved in OS were selected using GSE65071 dataset from the Gene Expression Omnibus (GEO) database and Gene Expression Profiling Interactive Analysis (GEPIA). Reverse transcription quantitative polymerase chain reaction (RT-qPCR) and Western blotting were conducted to detect miR-331-3p, MGAT1, the epithelial-mesenchymal transition (EMT), Bcl-2/Bax and Wnt/β-Catenin signaling pathways related proteins. Dual-luciferase reporter assay and TargetScan were used for validating interaction between MGAT1 mRNA and miR-331-3p. Biological effects of miR-331-3p and MGAT1 on OS cells were detected employing MTT, Transwell, wound healing and flow cytometry, respectively. MiR-331-3p was under-expressed in OS, and up-regulation or inhibition of its expression could significantly inhibit or promote the malignant phenotypes of OS cells. Furthermore, we found that MGAT1, a target of miR-331-3p, had elevated expression in OS. Interestingly, MGAT1 could partially alleviate the effect of miR-331-3p in vitro. Collectively, miR-331-3p acts as an critical tumor suppressor through inhibiting MGAT1, results in suppressed Wnt/β-Catenin pathway and decreased proliferation of OS cells; leads to increased apoptosis via Bcl-2/Bax pathway and inhibited migration and invasion ability via the EMT.

MTT assay

10.1080/21655979.2022.2083855

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Effect of Antisense Hypoxia-inducible Factor 1?? on Progression, Metastasis, and Chemosensitivity of Pancreatic Cancer

Pancreas (2006)

Qing Chang Renyi Qin Tao Huang Jun Gao Yanping Feng

Objectives: The aim of the study was to observe the effect of antisense hypoxia-inducible factor 1α (HIF-1α) on progression, metastasis, and chemosensitivity of pancreatic cancer. Methods: BxPc-3 cells transfected with antisense HIF-1α plasmid were exposed to 0.5% O2 for 4 hours. Expressions of HIF-1α, survivin, and β1 integrin were detected by reverse transcriptase -polymerase chain reaction and Western blotting. Growth inhibition rates and apoptosis rates of BxPc-3 cells under different dosages of chemotherapy agents (5-fluorouracil, doxorubicin, and gemcitabine) were measured by MTT colorimetric assay and flow cytometry. The migration of BxPc-3 cells was assayed using transwell cell culture chambers. Subcutaneous transplantation of BxPc-3 cells in nude mice for 8 weeks was to assess progression and metastasis of pancreatic cancer. Results: Expression of HIF-1α was obviously down-regulated, and at the same time, survivin and β1-integrin expressions were markedly down-regulated in the experimental group (P < 0.05). Higher dosages (100, 200, and 400 mg/L of 5-fluorouracil; 0.05, 0.075, and 0.1 mg/L of doxorubicin; and 10−9, 10−8, and 10−7 mol/L of gemcitabine) caused a greater increase of inhibition in the experimental group than in control (P < 0.05). The number of migrated BxPc-3 cells in the experimental group was far less than in control (P < 0.05). In vivo, the tumor size and weight in the experimental group were significantly lower than those in control (P < 0.05). Conclusion: Our data demonstrate that antisense HIF-1α inhibits expressions of survivin and β1 integrin, enhancing apoptosis in human pancreatic cancer cells and restraining the progression and metastasis of pancreatic cancer. Therefore, HIF-1α may play a very important role in progression, metastasis, and chemosensitivity of human pancreatic cancer. Blocking HIF-1α in pancreatic cancer cells may offer an avenue for gene therapy.

Survivin

Mitomycin C

10.1097/00006676-200604000-00010

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Citations (54)

Postnatal reduction of BDNF regulates the developmental remodeling of taste bud innervation

Developmental Biology (2015)

Tao Huang Liqun Ma Robin F. Krimm

Taste bud

Taste receptor

10.1016/j.ydbio.2015.07.006

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Citations (21)

Long non‑coding RNA ANRIL promotes the proliferation, migration and invasion of human osteosarcoma cells

Experimental and Therapeutic Medicine (2017)

Shuo Cheng Tao Huang Pengcheng Li Wei Zhang Zhihang Wang

The long antisense non‑coding RNA ANRIL is 3.8 kb in length and serves an important role in the tumorigenesis and progression of a number of malignancies. However, its function in human osteosarcoma remains unknown. The present study investigated the role of ANRIL in human osteosarcoma cell lines and clinical tumor samples. The expression of ANRIL was analyzed in 19 osteosarcoma and paired adjacent non‑cancerous tissues using reverse transcription‑quantitative polymerase chain reaction. Knockdown of ANRIL expression using lentivirus‑mediated small interfering RNA was performed to investigate the role of ANRIL in tumor proliferation and metastasis using MTT, colony formation and transwell assays. The results demonstrated that ANRIL expression was upregulated in osteosarcoma tissues when compared with ANCT samples. In addition, knockdown of ANRIL expression in vitro reduced cell proliferation and invasion. These results indicated that ANRIL is upregulated in osteosarcoma tissues, and may promote the proliferation and metastasis of osteosarcoma cells. Therefore, ANRIL may serve as a novel biomarker and target of novel therapies for the treatment of patients with osteosarcoma.

10.3892/etm.2017.5123

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Citations (12)