A5068959684- Intracerebral and Subarachnoid Hemorrhage Research
- Vascular Malformations Diagnosis and Treatment
- RNA modifications and cancer
- Epigenetics and DNA Methylation
- RNA Research and Splicing
- Intracranial Aneurysms: Treatment and Complications
- Cancer-related molecular mechanisms research
- Cancer Cells and Metastasis
- Ubiquitin and proteasome pathways
- Cell Adhesion Molecules Research
- Cervical Cancer and HPV Research
- Radiomics and Machine Learning in Medical Imaging
- Histone Deacetylase Inhibitors Research
- Pancreatic and Hepatic Oncology Research
- Immunotherapy and Immune Responses
- Wnt/β-catenin signaling in development and cancer
- Hippo pathway signaling and YAP/TAZ
- Galectins and Cancer Biology
- Helicobacter pylori-related gastroenterology studies
- Cancer-related gene regulation
- Autophagy in Disease and Therapy
- Thyroid Cancer Diagnosis and Treatment
Long Island University
2021-2022
New York University
2021-2022
Hebei North University
2021-2022
State Key Laboratory of Natural and Biomimetic Drugs
2018-2019
Peking University
2018-2019
Ministry of Education of the People's Republic of China
2018-2019
The Hippo signaling pathway plays a key role in development and cancer progression. However, molecules that intrinsically inhibit this are less well known. Here, we report the focal adhesion molecule Kindlin-2 inhibits by interacting with degrading MOB1 promoting interaction between E3 ligase praja2. thus phosphorylation of LATS1 YAP promotes translocation into nucleus, where it activates downstream target gene transcription. depletion Hippo/YAP alleviates renal fibrosis knockout mice...
Gastric cancer is a widespread and deadly malignancy among global digestive tract tumors, alarmingly ranking as the fifth most common in terms of incidence mortality. Our research, utilizing immunohistochemistry qRT-PCR, revealed significant upregulation YTHDF3 gastric tissues compared to adjacent non-cancerous tissues. This increased expression was found be closely associated with lymph node metastasis progression more advanced TNM stages patients. In vitro experiments demonstrated that...
Papillary thyroid cancer (PTC) is one of the most prevalent endocrine malignancies and associated with severe morbidity high mortality. This study aimed to explore role long non-coding RNA (lncRNA) SLC8A1 antisense 1 (SLC8A1-AS1) in pathogenesis PTC. In this study, we explored function SLC8A1-AS1 PTC progression. We observed that expression was downregulated clinical samples cell lines compared normal controls. Cell counting kit (CCK)-8 assays demonstrated overexpression significantly...
The loss function of cerebral cavernous malformation (CCM) genes leads to most CCM lesions characterized by enlarged leaking vascular in the brain. Although we previously showed that NOGOB receptor (NGBR) knockout endothelial cells (ECs) results cerebrovascular mouse embryo, molecular mechanism which NGBR regulates CCM1/2 expression has not been elucidated. Here, show genetic depletion Ngbr ECs at both postnatal and adult stages deficiency such as vessels, blood-brain-barrier...
Abnormal expression of trefoil factor 3 (TFF3) in breast, stomach, and colon tumors may be related to the occurrence tumors, suggesting its role angiogenesis. In this study, aim was explore TFF3 thyroid cancer.TFF3 analysis performed via GEPIA RT-PCR. To effects on cancer cell motility, function assays were performed. Furthermore, GSEA pathway western blot used mechanism by which represses progression cells.Here, we showed that low level is nodal metastasis. The patients with worse...
To investigate the detection rate and metastasis of delphain lymph node （DLN）in thyroid papillary adenocarcinoma（PTC） to analyze risk factors for DLN metastasis.
Cerebral cavernous malformations (CCMs) are enlarged leaking vascular lesions in the brain caused by loss-of-function mutations CCM1/2/3 genes or loss of expression. Although we previously showed that Nogo-B receptor (NgBR) knockout endothelial cells (ECs) results CCMs-like cerebrovascular mouse embryo, molecular mechanism which NgBR regulates CCM1/2 expression has not been elucidated. Here, show temporal genetic depletion ECs at both postnatal and adult stages deficiency consequently such...
Cerebral cavernous malformations (CCMs) are enlarged leaking vascular lesions in the brain caused by loss-of-function mutations CCM1/2/3 genes or loss of expression. Although we previously showed that Nogo-B receptor (NgBR) knockout endothelial cells (ECs) results CCMs-like cerebrovascular mouse embryo, molecular mechanism which NgBR regulates CCM1/2 expression has not been elucidated. Here, show temporal genetic depletion ECs at both postnatal and adult stages deficiency consequently such...