Fan Zhang

Army Medical University

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Anil K. Sood

The University of Texas MD Anderson Cancer Center

Zhaobing Qin

First Affiliated Hospital of Zhengzhou University

Gordon B. Mills

Oregon Health & Science University

Sunila Pradeep

Medical College of Wisconsin

Qipeng Zhang

Nanjing Drum Tower Hospital

Yiling Lu

The University of Texas MD Anderson Cancer Center

Jing Li

First Affiliated Hospital of Xi'an Jiaotong University

Elsa R. Flores

Moffitt Cancer Center

Liangsheng Lu

Children's Hospital of Fudan University

Lu Xing

Northern Jiangsu People's Hospital

Cooperative Institutions

Harbin Medical University

Capital Medical University

The University of Texas MD Anderson Cancer Center

Huazhong University of Science and Technology

Shanghai Jiao Tong University

Nanjing University

Army Medical University

Southern Medical University

Sun Yat-sen University

Sichuan University

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MiRNA-219a-1-3p inhibits the malignant progression of gastric cancer and is regulated by DNA methylation

ONCOLOGIE (2023)

Min Luo Jian Tang Ying Zhu Liping Wu Hu Fu

Abstract Objective Worldwide, gastric cancer (GC) is one of primary reasons for cancer-related deaths. However, the pathogenic mechanism underlying GC remains to be fully understood. MicroRNAs are momentous regulators of diverse biological progression in cancer. Even though the ability of miR-219a-1-3p to inhibit malignant progression in pancreatic cancer have been previously reported, its role in GC remains to be elucidated. Methods Quantitative real-time PCR (qRT-PCR) was performed to measure miR-219a-1-3p expression levels in collected GC samples (n=98) and paired nearby non-tumor tissues. Cell proliferation, migration, and invasion assays were then conducted to explain the biological influences of miR-219a-1-3p in vitro . In vivo effects were confirmed by subcutaneously injecting miR-219a-1-3p overexpressing MGC-803 cells into nude mice. Methylation-specific PCR was employed to evaluate the CpG island upstream methylation condition of miR-219a-1-3p in collected clinical tissues (n=22), GC cell lines and GES-1 cells. GC cells were supplemented with 5-aza-2′-deoxycytidine to identify the miR-219a-1-3p expression changes using qRT-PCR. Results The miR-219a-1-3p expression was obviously suppressed in GC tissues relation to nearby non-tumor tissues, along with in GC cell lines in comparison to GES-1. Moreover, in vivo and in vitro functional evaluations indicated the function of miR-219a-1-3p in inhibiting the malignant characteristics of GC cells. Mechanistically, MiR-219a-1-3p expression was partly regulated utilizing DNA hypermethylation in GCs. In addition, overexpression of miR-219a-1-3p inhibited PI3K/AKT signaling. Conclusions MiR-219a-1-3p might function as a tumor suppressor in GC, and our investigation creates a foundation to diagnose of GC.

CpG site

10.1515/oncologie-2023-0024

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Effect of icariine on the formations of mesenchymal stem cells of umbilical cord to osteoblasts

Zhonghua xianwei waike zazhi (2011)

Xuejian Wu Fan Zhang Yang Song

Objective To study the biological effect of Icariine on human umbilical cord derived mesenchymal stem cells（huCMSCs） and inducing them to differentiate into osteoblasts. Methods MSCs were isolated and expanded in vitro and their surface antigens of huCMSCs were detected by immunohistochemistry. HuCMSCs were assigned into two groups. In the blank control group, huMSCs were incubated in basic medium. In the experimental group huMSCs were incubated in Icariine medium, The proliferation and differentiation of huMSCs were examined by inverted microscope, Alkaline phosphatase （ALP） staining and the determination of ALP activities. Results HuCMSCs were strongly positive for CD44, and negative for CD34; strongly positive expression for ALP and calcium deposition was detected from the second day to the fourth day in Icariine group; blank control group and Icariine group had significant differences （P 〈 0.05）.Conclusion HuCMSCs can be successfully cultured from the adherent tissue pieces, Icariine enhances proliferation and osteogenic differentiation of huCMSCs and be used as an osteoinductive factor. Key words: Umbilical cord; Mesenchymal stem cells; Icariine; Osteoblasts

Cord lining

10.3760/cma.j.issn.1001-2036.2011.01.019

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Multiple sclerosis patient-derived CSF induces transcriptional changes in proliferating oligodendrocyte progenitors

Multiple Sclerosis Journal (2015)

Jeffery D. Haines Óscar G. Vidaurre Fan Zhang Ángela L. Riffo‐Campos Josefa Castillo

Background: Cerebrospinal fluid (CSF) is in contact with brain parenchyma and ventricles, and its composition might influence the cellular physiology of oligodendrocyte progenitor cells (OPCs) thereby contributing to multiple sclerosis (MS) disease pathogenesis. Objective: To identify the transcriptional changes that distinguish the transcriptional response induced in proliferating rat OPCs upon exposure to CSF from primary progressive multiple sclerosis (PPMS) or relapsing remitting multiple sclerosis (RRMS) patients and other neurological controls. Methods: We performed gene microarray analysis of OPCs exposed to CSF from neurological controls, or definitive RRMS or PPMS disease course. Results were confirmed by quantitative reverse transcriptase polymerase chain reaction, immunocytochemistry and western blot of cultured cells, and validated in human brain specimens. Results: We identified common and unique oligodendrocyte genes for each treatment group. Exposure to CSF from PPMS uniquely induced branching of cultured progenitors and related transcriptional changes, including upregulation ( P<0.05) of the adhesion molecule GALECTIN-3/ Lgals3, which was also detected at the protein level in brain specimens from PPMS patients. This pattern of gene expression was distinct from the transcriptional programme of oligodendrocyte differentiation during development. Conclusions: Despite evidence of morphological differentiation induced by exposure to CSF of PPMS patients, the overall transcriptional response elicited in cultured OPCs was consistent with the activation of an aberrant transcriptional programme.

Parenchyma

10.1177/1352458515573094

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Preliminary study of microRNA-126 as a novel therapeutic target for primary hypertension

International Journal of Molecular Medicine (2018)

Jia Liu Jiamei Liu Ling‐Ying Shi Fan Zhang Liping Yu

The present study aimed to explore microRNA-126 (miR-126) as a novel therapeutic target for primary hypertension. The lentiviral vector containing human immunodeficiency virus 1 (HIV‑1), the miR‑126 gene knockdown viral vector (lenti-miR-126-KD), and control lentiviral vector (lenti‑scramble‑miR) were constructed. Spontaneously hypertensive rats were randomly divided into 4 groups, which received a high dose of lenti‑miR‑126‑KD (1x108, n=5), low dose of lenti‑miR‑126‑KD (1x107, n=6), scramble‑miR (5x107, n=6), and PBS (n=6). Lentiviral vectors were injected into the tail vein. Data on the systolic blood pressure, diastolic pressure, mean arterial pressure, and heart rate were collected weekly. After 8 weeks of virus administration, the distribution of lentiviral vectors in different tissues was observed by fluorescence microscopy. Picric acid Sirius red and H&E staining were used to observe the target organ damage, and the ELISA kit was used to determine the serum nitric oxide (NO) content. The lentiviral vector was found to be constructed successfully. Eight weeks after the lentiviral vector injection, green fluorescent protein was observed in different tissues in each group. The blood pressure and heart rate were not significantly altered after lentiviral vector injection (P>0.05). No significant differences in the heart‑to‑body weight ratio among the four groups were observed (P=0.23). Picric acid Sirius red and H&E staining revealed that there was no significant difference in morphology among the four groups. No significant difference in the serum NO level among the four groups was noted (P=0.23). The miR‑126 gene knockdown lentiviral vector was constructed successfully. No significant antihypertensive effect was observed by the knockdown of miR‑126 for the treatment of primary hypertension. The target organs were not protected significantly after the treatment. The increased level of miR‑126 expression in hypertensive patients may be due to a compensatory mechanism.

Sirius Red

10.3892/ijmm.2018.3420

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Significantly altered expression of miR-511-3p and its target AKT3 has negative prognostic value in human prostate cancer

Biochimie (2017)

Fan Zhang Zhongjun Wu

Value (mathematics)

Expression (computer science)

AKT3

10.1016/j.biochi.2017.06.007

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Citations (23)

MiR-599 targeting TOP2A inhibits the malignancy of bladder cancer cells

Biochemical and Biophysical Research Communications (2021)

Fan Zhang Hong Wu

10.1016/j.bbrc.2021.06.069

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Citations (13)

An integrative framework to identify cell death-related microRNAs in esophageal squamous cell carcinoma

Oncotarget (2016)

Bingli Wu Dong Wang Wenjing Bai Fan Zhang Xing Zhao

Cell death is a critical biological process involved in many important functions, and defects in this system are usually linked with numerous human diseases including cancers. Esophageal squamous cell carcinoma is one of the most chemo- and biological therapy resistant cancers. Based on knowledge repository and four miRNAs profiling data, we proposed a general framework to hunt for cell death miRNAs in a context dependent manner. We predicted 12 candidate miRNAs from hundreds of others. Follow-up experimental verification of 7 miRNAs indicated at least 3 miRNAs (MIR20b, MIR498 and MIR196) were involved in both apoptosis and autophagy processes. These results indicated miRNAs intimately connected the two cell death modules in esophageal squamous cell carcinoma. This integrative framework can also be easily extended to identify miRNAs in other key cellular signaling pathways or may find conditional specific miRNAs in other cancer types.

10.18632/oncotarget.10779

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Citations (8)

[Prediction of the microRNAs related to cardiovascular diseases by bioinformatics].

Fan Zhang Ming Lu Qi-peng Zhang Fuchun Zhang Wei Gao

To predict the microRNAs (miRNAs) related to cardiovascular diseases.Bioinformatics was used to find all cardiovascular disease related and cardiovascular function related protein-coding genes, and miRNAs were identified that localized the same transcription units as the above genes. Then other cardiovascular disease related miRNAs were identified by an miRNAs set and family analysis and Gene Ontology(GO).Twenty potential cardiovascular disease related miRNAs were predicted from 626 cardiovascular disease related miRNAs, five of which had been confirmed by experiments.This study is of great help for the diagnosis and research of cardiovascular diseases, but the final conclusion need to be confirmed by experiments.

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Detection of Phenolic Metabolites of Styrene in Mouse Liver and Lung Microsomal Incubations

Drug Metabolism and Disposition (2010)

Shuijie Shen Fan Zhang Lingbo Gao Su Zeng Jiang Zheng

Metabolic activation is considered to be a critical step for styrene-induced pulmonary toxicity. Styrene-7,8-oxide is a primary oxidative metabolite generated by vinyl epoxidation of styrene. In addition, urinary 4-vinylphenol (4-VP), a phenolic metabolite formed by aromatic hydroxylation, has been detected in workers and experimental animals after exposure to styrene. In the present study, new oxidative metabolites of styrene, including 2-vinylphenol (2-VP), 3-vinylphenol (3-VP), vinyl-1,4-hydroquinone, and 2-hydroxystyrene glycol were detected in mouse liver microsomal incubations. The production rates of 2-VP, 3-VP, 4-VP, and styrene glycol were 0.0527 ± 0.0045, 0.0019 ± 0.0006, 0.0053 ± 0.0002, and 4.42 ± 0.33 nmol/(min · mg protein) in mouse liver microsomes, respectively. Both disulfiram (100 μM) and 5-phenyl-1-pentyne (5 μM) significantly inhibited the formation of the VPs and styrene glycol. 2-VP, 3-VP, and 4-VP were metabolized in mouse liver microsomes at rates of 2.50 ± 0.30, 2.63 ± 0.13, and 3.45 ± 0.11 nmol/(min · mg protein), respectively. The three VPs were further metabolized to vinylcatechols and/or vinyl-1,4-hydroquinone and the corresponding glycols. Pulmonary toxicity of 2-VP, 3-VP, and 4-VP was evaluated in CD-1 mice, and 4-VP was found to be more toxic than 2-VP and 3-VP.

Hydroquinone

Hydroxylation

Styrene oxide

Microsoma

10.1124/dmd.110.033522

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DNA Methylation Mediated Downregulation of miR-449c Controls Osteosarcoma Cell Cycle Progression by Directly Targeting Oncogene c-Myc

International Journal of Biological Sciences (2017)

Qing Li Hua Li Xueling Zhao Bing Wang Lin Zhang

MicroRNAs (miRNAs) are critical regulators of gene expression, and they have broad roles in the pathogenesis of different diseases including cancer.Limited studies and expression profiles of miRNAs are available in human osteosarcoma cells.By applying a miRNA microarray analysis, we observed a number of miRNAs with abnormal expression in cancerous tissues from osteosarcoma patients.Of particular interest in this study was miR-449c, which was significantly downregulated in osteosarcoma cells and patients, and its expression was negatively correlated with tumor size and tumor MSTS stages.Ectopic expression of miR-449c significantly inhibited osteosarcoma cell proliferation and colony formation ability, and caused cell cycle arrest at the G1 phase.Further analysis identified that miR-449c was able to directly target the oncogene c-Myc and negatively regulated its expression.Overexpression of c-Myc partially reversed miR-449c-mimic-inhibited cell proliferation and colony formation.Moreover, DNA hypermethylation was observed in two CpG islands adjacent to the genomic locus of miR-449c in osteosarcoma cells.Conversely, treatment with the DNA methylation inhibitor AZA caused induction of miR-449c.In conclusion, our results support a model that DNA methylation mediates downregulation of miR-449c, diminishing miR-449c mediated inhibition of c-Myc and thus leading to the activation of downstream targets, eventually contributing to osteosarcoma tumorigenesis.

Ectopic expression

CpG site

DNMT1

10.7150/ijbs.19476

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Citations (31)