Minglin Zhu
Current Organizations / Institutes
The organizations/institutes from the scholar's latest article
Previous Organizations / Institutes
The organizations / institutes from the scholar's other articles in the past ten years
Minglin Zhu has a total of 23 co-authors. Here are the top co-authors by number of shared publications:
- Gaofeng Pan
Cardiovascular Surgery, Zhongnan Hospital of Wuhan University, Wuhan, China
2 shared publications - Hexiao Tang
Department of Thoracic Surgery, ZhongNan Hospital of Wuhan University, Wuhan, China
2 shared publications - Jinping Zhao
Department of Thoracic Surgery, ZhongNan Hospital of Wuhan University, Wuhan, China
2 shared publications - Lecai Xiong
Department of Thoracic and Cardiovascular Surgery Zhongnan Hospital of Wuhan University 430071 Wuhan China
2 shared publications - Li Zhang
Department of Thoracic and Cardiovascular Surgery Zhongnan Hospital of Wuhan University 430071 Wuhan China
2 shared publications - Ming Xu
Department of Thoracic Surgery, ZhongNan Hospital of Wuhan University, Wuhan, China
2 shared publications
Latest Publications
- Top Cited PapersOpen Access
- 11 May 2024
- Published by Springer Nature in Cellular and Molecular Life Sciences
- Vol. 81 (1) , 1-25
Circular RNAs in EMT-driven metastasis regulation: modulation of cancer cell plasticity, tumorigenesis and therapy resistance
The non-coding RNAs comprise a large part of human genome lack of capacity in encoding functional proteins. Among various members of non-coding RNAs, the circular RNAs (circRNAs) have been of importance in the pathogenesis of human diseases, especially cancer. The circRNAs have a unique closed loop structure and due to their stability, they are potential diagnostic and prognostic factors in cancer. The increasing evidences have highlighted the role of circRNAs in the modulation of proliferation and metastasis of cancer cells. On the other hand, metastasis has been responsible for up to 90% of cancer-related deaths in patients, requiring more investigation regarding the underlying mechanisms modulating this mechanism. EMT enhances metastasis and invasion of tumor cells, and can trigger resistance to therapy. The cells demonstrate dynamic changes during EMT including transformation from epithelial phenotype into mesenchymal phenotype and increase in N-cadherin and vimentin levels. The process of EMT is reversible and its reprogramming can disrupt the progression of tumor cells. The aim of current review is to understanding the interaction of circRNAs and EMT in human cancers and such interaction is beyond the regulation of cancer metastasis and can affect the response of tumor cells to chemotherapy and radiotherapy. The onco-suppressor circRNAs inhibit EMT, while the tumor-promoting circRNAs mediate EMT for acceleration of carcinogenesis. Moreover, the EMT-inducing transcription factors can be controlled by circRNAs in different human tumors.
- 11 May 2024
- Published by Springer Nature in Cellular and Molecular Life Sciences
- Vol. 81 (1) , 1-25
Top Cited PapersOpen AccessCircular RNAs in EMT-driven metastasis regulation: modulation of cancer cell plasticity, tumorigenesis and therapy resistance
The non-coding RNAs comprise a large part of human genome lack of capacity in encoding functional proteins. Among various members of non-coding RNAs, the circular RNAs (circRNAs) have been of importance in the pathogenesis of human diseases, especially cancer. The circRNAs have a unique closed loop structure and due to their stability, they are potential diagnostic and prognostic factors in cancer. The increasing evidences have highlighted the role of circRNAs in the modulation of proliferation and metastasis of cancer cells. On the other hand, metastasis has been responsible for up to 90% of cancer-related deaths in patients, requiring more investigation regarding the underlying mechanisms modulating this mechanism. EMT enhances metastasis and invasion of tumor cells, and can trigger resistance to therapy. The cells demonstrate dynamic changes during EMT including transformation from epithelial phenotype into mesenchymal phenotype and increase in N-cadherin and vimentin levels. The process of EMT is reversible and its reprogramming can disrupt the progression of tumor cells. The aim of current review is to understanding the interaction of circRNAs and EMT in human cancers and such interaction is beyond the regulation of cancer metastasis and can affect the response of tumor cells to chemotherapy and radiotherapy. The onco-suppressor circRNAs inhibit EMT, while the tumor-promoting circRNAs mediate EMT for acceleration of carcinogenesis. Moreover, the EMT-inducing transcription factors can be controlled by circRNAs in different human tumors.
- Open Access
- 5 May 2020
- Published by MDPI AG in Preprints.org
Complete Excision of the Jejunum and Vessels for the Treatment of Esophageal Cancer
Herein, we reported a case of complete excision of the jejunum for the treatment of esophageal cancer. A 62-year-old male was admitted with complaints of “difficulty in eating for one month and chest pain for 10 days". For complete gastrectomy and colonic polyposis, we chose the jejunum. We completely excised the jejunum and its vessels, anastomosed to the esophageal tumor resection, with no significant complications. This case showed that complete excision of the jejunum with bowel and vessels is an alternative surgical method for the treatment of esophageal cancer with free bowel shortage and no torsion of blood vessels.
- 5 May 2020
- Published by MDPI AG in Preprints.org
Open AccessComplete Excision of the Jejunum and Vessels for the Treatment of Esophageal Cancer
Herein, we reported a case of complete excision of the jejunum for the treatment of esophageal cancer. A 62-year-old male was admitted with complaints of “difficulty in eating for one month and chest pain for 10 days". For complete gastrectomy and colonic polyposis, we chose the jejunum. We completely excised the jejunum and its vessels, anastomosed to the esophageal tumor resection, with no significant complications. This case showed that complete excision of the jejunum with bowel and vessels is an alternative surgical method for the treatment of esophageal cancer with free bowel shortage and no torsion of blood vessels.
- Open Access
- 5 May 2020
- Published by MDPI AG in Preprints.org
Knockdown of CENPF Inhibits the Progression of Lung Adenocarcinoma Mediated by ERβ2/5 Pathway
The signal transduction pathways of estrogen receptors (ER) mainly includes gene pathway and non-gene pathway. Studies have shown that the gene pathway of ER is related with the expression of nuclear proteins, and this is the key issue for our current research. With the GEO database analysis, Human centromere protein F (CENPF) is highly expressed in adenocarcinoma of lung (LUAD), and the co-expression of CENPF and ERβ was found in the nucleus of LUAD cells. Meanwhile, CENPF and ERβ2/5 were related with T stage and poor prognosis (P<0.05). Knockdown of CENPF gene significantly inhibited the biological effects of LUAD cells, the tumor growth of mice and the expression of ERβ2/5 (P<0.05). Further, group experiments showed that knockdown CENPF inhibits biological effects of LUAD cells mediated by ERβ pathway. All the results indicated that both CENPF and ERβ2/5 play important roles in the progression of LUAD, and knockdown of CENPF can inhibit the progression of LUAD by inhibiting the expression of ER2/5. Thus, the development of inhibitors against ERβ2/5 subtype and CENPF remained more effective in improving the therapeutic effect of LUAD.
- 5 May 2020
- Published by MDPI AG in Preprints.org
Open AccessKnockdown of CENPF Inhibits the Progression of Lung Adenocarcinoma Mediated by ERβ2/5 Pathway
The signal transduction pathways of estrogen receptors (ER) mainly includes gene pathway and non-gene pathway. Studies have shown that the gene pathway of ER is related with the expression of nuclear proteins, and this is the key issue for our current research. With the GEO database analysis, Human centromere protein F (CENPF) is highly expressed in adenocarcinoma of lung (LUAD), and the co-expression of CENPF and ERβ was found in the nucleus of LUAD cells. Meanwhile, CENPF and ERβ2/5 were related with T stage and poor prognosis (P<0.05). Knockdown of CENPF gene significantly inhibited the biological effects of LUAD cells, the tumor growth of mice and the expression of ERβ2/5 (P<0.05). Further, group experiments showed that knockdown CENPF inhibits biological effects of LUAD cells mediated by ERβ pathway. All the results indicated that both CENPF and ERβ2/5 play important roles in the progression of LUAD, and knockdown of CENPF can inhibit the progression of LUAD by inhibiting the expression of ER2/5. Thus, the development of inhibitors against ERβ2/5 subtype and CENPF remained more effective in improving the therapeutic effect of LUAD.