董培新

董 培新（ドン バイシン; Dong Peixin）は、日本の癌研究者、医学博士。北海道大学医学部。

 略歴 
 1997年6月 中国ハルビン医科大学卒業
 1997年8月 中国ハルビン医科大学付属黒龍江省電力病院婦人科医員
 2002年10月 福岡大学医学部産婦人科研究員
 2004年4月 北海道大学大学院医学研究科婦人科専攻入学
 2008年3月 北海道大学大学院医学研究科婦人科専攻終了(博士号取得)
 2008年4月 中国上海復旦大学付属病院産婦人科病院助手
 2009年4月 中国上海復旦大学付属病院産婦人科病院講師
 2010年4月 北海道大学医学研究科産婦人科学分野

 受賞歴 
 2011年度 北海道産科婦人科学会賞（October 28, 2012）受賞
 2015年度 北海道大学研究総長賞（February 3, 2016）受賞

 所属学会 
 日本産婦人科学会（会員：2011年～現在）
北海道産婦人科学会（会員：2011年～現在）
 日本RNA学会（会員：2014年～現在）

 社会における活動 
国際誌Editorial Board Member：
 Journal of Cancer Research & Therapy、2013年～2015年
 Cancer Growth and Metastasis、2013年～2015年
 Austin Journal of Women’s Health、2014年～現在
 Women's Health Research、2017～現在
国際誌reviewer：
 Oncotarget
 Scientific Reports
 Journal of Translational Medicine
 Gynecologic Oncology
 BMC Cancer
 Journal of Experimental & Clinical Cancer Research
 FEBS Letters
 Molecular and cellular biochemistry
 International Journal of Gynecology & Obstetrics

 専攻分野 
 癌転移
 婦人科癌; endometrial carcinoma; cervical cancer; ovarian cancer
 microRNA
 EMT: epithelial to mesenchymal transition (EMT)
 Twist1 gene, a critical EMT inducer in endometrial cancer
 :en:Cervical_cancer cervical cancer
 p53: TP53, tumor suppressor in human tumors
 endometrial cancer
 ovarian cancer
 miR-194 is a tumor suppressor in endometrial cancer
 Prognostic significance of miR-194 in endometrial cancer
 miR-130b in endometrial cancer
 miR-101 is key tumor suppressor in both type I and type II endometrial cancer
 IQGAP1 is novel oncogene in endometrial cancer and ovarian cancer
 miR-106b acts as tumor suppressor in aggressive in endometrial cancer
 KLF17 gene induces EMT in endometrial cancer
 miR-31 functions as an oncogene by suppressing Hippo tumor suppressor pathway in endometrial cancer
 MiR-137 and miR-34a directly target Snail and inhibit EMT, invasion and sphere-forming ability of ovarian cancer cells. 35, Article number: 132 
 iASPP and p53 in human tumors
 miRNA-mediated PI3K/AKT signaling in endometrial cancer
 miRNA-124 directly targets and inhibits IQGAP1 expression in endometrial cancer
 EZH2 induces Twist expression by repressing miR-361 expression in aggressive type II endometrial cancer
 CRISPR/Cas9 vector mediated miR-21 gene editing inhibits the epithelial to mesenchymal transition in ovarian cancer cells
 lentiviral CRISPR/Cas9-mediated disruption of miR-21 inhibits EMT in ovarian cancer cells
 miR-124 binds to and suppresses oncogene iASPP expression in cervical cancer
 iASPP induces EMT and cisplatin resistance through miR-20a-FBXL5/BTG3 signaling in cervical cancer
 p53 gain of function mutations promote endometrial cancer progression and metastasis
 EZH2, MCL-1 and FOS gene are important oncogenes and EMT inducers in endometrial cancer
 CRISPR/Cas9 and and genome editing
 ZEB1 acts as a novel EMT inducer in endometrial cancer
 BMI-1 gene functions as a important EMT inducer in endometrial cancer cells
 Musashi-2 (MSI-2) has a crucial role in promoting cervical cancer metastasis
 PD-L1 is a critical oncogenic factor in cervical cancer progression, and miR-140/142/340/383 regulate the expression of PD-L1 in cervical cancer
 Exploring lncRNA-Mediated Regulatory Networks in Endometrial Cancer
 Long noncoding RNA NEAT1 drives aggressive endometrial cancer progression via miR-361-regulated networks involving STAT3 and tumor microenvironment-related genes
 B7H3 As a Promoter of Metastasis and Promising Therapeutic Target
 miR-203 inhibits ovarian tumor metastasis by targeting BIRC5 and attenuating the TGFβ pathway
 KLF4 expression enhances the efficacy of chemotherapy drugs in ovarian cancer cells
 Lentiviral vector mediated-ASAP1 expression promotes epithelial to mesenchymal transition in ovarian cancer cells
 miR-34a, miR-424 and miR-513 inhibit MMSET expression to repress endometrial cancer cell invasion and sphere formation
 Molecular-targeted therapies and precision medicine for endometrial cancer
 Lentiviral CRISPR/Cas9 nickase vector mediated BIRC5 editing inhibits epithelial to mesenchymal transition in ovarian cancer cells
 The Expression, Functions and Mechanisms of Circular RNAs in Gynecological Cancers
 Ovarian Primary and Metastatic Tumors Suppressed by Survivin Knockout or a Novel Survivin Inhibitor
 
 LncRNA NEAT1-mediated miR-361 downregulation contributes to EMT of cervical cancer cells via increasing HSP90 expression: Epithelial-mesenchymal transition (EMT) is a key process contributing to cervical cancer (CC) metastasis, and microRNAs (miRNAs) modulate the expression of genes implicated in EMT. However, the accurate role of miR-361 in CC-associated EMT and the mechanisms underlying its function in CC remains largely unknown. The functional roles of miR-361 in CC cells were explored by a series of cell functional assays. Luciferase reporter assays were used to demonstrate the potential interaction between miR-361, HSP90, and long non-coding RNA (lncRNA) NEAT1. We detected a reduction of miR-361 expression in CC tissues compared with normal tissues, and miR-361 overexpression inhibited invasion and EMT phenotypes of CC cells by directly targeting a key EMT activator HSP90. Additionally, we detected significantly higher levels of HSP90 in CC tissues compared with normal tissues, and high expression of HSP90 predicted a poorer prognosis. We further identified NEAT1 as a significantly upregulated lncRNA in CC tissues and high expression of NEAT1 was associated with worse survival in CC patients. NEAT1 directly repressed miR-361 expression and played an oncogenic role in CC cell invasion and sphere formation. Conclusions: These results demonstrated that miR-361 directly targets HSP90 to inhibit the invasion and EMT features, and NEAT1 functions as an oncogenic lncRNA that suppresses miR-361 expression and induces EMT and sphere formation in CC cells, thus providing critical insights into the molecular pathways operating in this malignancy.
 MicroRNA-361: A Multifaceted Player Regulating Tumor Aggressiveness and Tumor Microenvironment Formation
 PD-L1 Is a Tumor Suppressor in Aggressive Endometrial Cancer Cells and Its Expression Is Regulated by miR-216a and lncRNA MEG3
 Background: Poorly differentiated endometrioid adenocarcinoma and serous adenocarcinoma represent an aggressive subtype of endometrial cancer (EC). Programmed death-ligand-1 (PD-L1) was known to exhibit a tumor cell-intrinsic function in mediating immune-independent tumor progression. However, the functional relevance of tumor cell-intrinsic PD-L1 expression in aggressive EC cells and the mechanisms regulating its expression remain unknown. Methods: PD-L1 expression in 65 EC tissues and 18 normal endometrium samples was analyzed using immunohistochemical staining. The effects of PD-L1 on aggressive EC cell growth, migration and invasion were investigated by cell functional assays. Luciferase reporter assays were used to reveal the microRNA-216a (miR-216a)-dependent mechanism modulating the expression of PD-L1. Results: Positive PD-L1 expression was identified in 84% of benign cases but only in 12% of the EC samples, and the staining levels of PD-L1 in EC tissues were significantly lower than those in the normal tissues. Higher PD-L1 expression predicts favorable survival in EC. Ectopic expression of PD-L1 in aggressive EC cells results in decreased cell proliferation and the loss of mesenchymal phenotypes. Mechanistically, PD-L1 exerts the anti-tumor effects by downregulating MCL-1 expression. We found that PD-L1 levels in aggressive EC cells are regulated by miR-216a, which directly targets PD-L1. We further identified a mechanism whereby the long non-coding RNA MEG3 represses the expression of miR-216a, thereby leading to increased PD-L1 expression and significant inhibition of cell migration and invasion. Conclusion: These results reveal an unappreciated tumor cell-intrinsic role for PD-L1 as a tumor suppressor in aggressive EC cells, and identify MEG3 and miR-216a as upstream regulators of PD-L1.

 Research Topics 
 microRNAs are novel prognostic biomarkers and EMT modulators, and act as either oncogeic miRNAs (OncomiRs) or tumor suppressors in endometrial cancer.
 Mutant p53 Gain-of-Function in Cancer: Besides the dominant negative effects upon wild type p53, increasing evidence suggests that p53 mutations acquire additional oncogenic functions, such as a gain-of-function (GOF), which actively drive cells toward invasion and metastasis7 through transactivation or transrepression of a large set of genes involved in regulation of cell adhesion, migration, and proliferation.
 Restoration of tumor suppressor miRNAs: The loss or down-regulation of a tumor suppressor miRNA could be overcome by the restoration of these silenced miRNAs.
 Blocking oncogenic miRNAs: Another strategy to target miRNA expression in cancer is to block the expression of an oncogenic miRNA.
 CRISPR/Cas9-Mediated Genome Editing of Epigenetic Factors for Cancer Therapy.
 Interconnection between EMT and stemness in gynecological cancers.
 miRNAs regulates endometrial cancer metastasis through modulating tumor microenvironment.