董培新
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 (2016)
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
Yue, Junming and Du, Ziyun and Zhou, Fu-Ming and Dong, Peixin and Pfeffer, Lawrence M「Applications of CRSIPR/Cas9 in Cancer Research」『Cancer Medicine & Anti Cancer Drugs』第1巻第1号、OMICS International、2016年3月、1000103頁、NAID 120005752854。
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.