ResearcherFirst Hospital of China Medical UniversityNo recent work listed
Rongxian Cao
Matched on OpenAlex author ID A5017669872. Sources: OpenAlex.
Their work
- Papers
- 7
- Trials
- 0
- Grants
- 0
- Labs led
- 0
- Collaborators
- 10
2020: 5 papers · 2021: none · 2022: 2 papers
Papers 7
- Numb-PRRL promotes TGF-β1- and EGF-induced epithelial-to-mesenchymal transition in pancreatic cancer. Co-author DOI 10.1038/s41419-022-04609-y↗
- Down-regulation of MSMO1 promotes the development and progression of pancreatic cancer. Co-author DOI 10.7150/jca.73112↗
- Musashi2 promotes the progression of pancreatic cancer through a novel ISYNA1-p21/ZEB-1 pathway. Co-author DOI 10.1111/jcmm.15676↗
- Correction to: Musashi2 promotes EGF-induced EMT in pancreatic cancer via ZEB1-ERK/MAPK signaling. Co-author DOI 10.1186/s13046-020-01663-2↗
- Calreticulin promotes EMT in pancreatic cancer via mediating Ca2+ dependent acute and chronic endoplasmic reticulum stress. Co-author DOI 10.1186/s13046-020-01702-y↗
- Musashi2 promotes EGF-induced EMT in pancreatic cancer via ZEB1-ERK/MAPK signaling. Co-author DOI 10.1186/s13046-020-1521-4↗
- CPA4 Promotes EMT in Pancreatic Cancer via Stimulating PI3K-AKT-mTOR Signaling. Co-author DOI 10.2147/ott.s257057↗
Closest collaborators
The 10 strongest of 10 by collab_strength@1: shared papers, trials and grants, recent and small-team work weighing most.
- Weiwei Sheng · 6 shared papers, 2020–2022 · strength 0.80
- Paper Numb-PRRL promotes TGF-β1- and EGF-induced epithelial-to-mesenchymal transition in pancreatic cancer. DOI 10.1038/s41419-022-04609-y↗
- Paper Down-regulation of MSMO1 promotes the development and progression of pancreatic cancer. DOI 10.7150/jca.73112↗
- Paper Musashi2 promotes the progression of pancreatic cancer through a novel ISYNA1-p21/ZEB-1 pathway. DOI 10.1111/jcmm.15676↗
- Ming Dong · 6 shared papers, 2020–2022 · strength 0.80
- Paper Numb-PRRL promotes TGF-β1- and EGF-induced epithelial-to-mesenchymal transition in pancreatic cancer. DOI 10.1038/s41419-022-04609-y↗
- Paper Down-regulation of MSMO1 promotes the development and progression of pancreatic cancer. DOI 10.7150/jca.73112↗
- Paper Musashi2 promotes the progression of pancreatic cancer through a novel ISYNA1-p21/ZEB-1 pathway. DOI 10.1111/jcmm.15676↗
- Guosen Wang · 4 shared papers, 2020 · strength 0.43
- Paper Musashi2 promotes the progression of pancreatic cancer through a novel ISYNA1-p21/ZEB-1 pathway. DOI 10.1111/jcmm.15676↗
- Paper Correction to: Musashi2 promotes EGF-induced EMT in pancreatic cancer via ZEB1-ERK/MAPK signaling. DOI 10.1186/s13046-020-01663-2↗
- Paper Musashi2 promotes EGF-induced EMT in pancreatic cancer via ZEB1-ERK/MAPK signaling. DOI 10.1186/s13046-020-1521-4↗
- Chao Jia · 4 shared papers, 2020 · strength 0.43
- Paper Musashi2 promotes the progression of pancreatic cancer through a novel ISYNA1-p21/ZEB-1 pathway. DOI 10.1111/jcmm.15676↗
- Paper Correction to: Musashi2 promotes EGF-induced EMT in pancreatic cancer via ZEB1-ERK/MAPK signaling. DOI 10.1186/s13046-020-01663-2↗
- Paper Musashi2 promotes EGF-induced EMT in pancreatic cancer via ZEB1-ERK/MAPK signaling. DOI 10.1186/s13046-020-1521-4↗
- Jian Hua Sun · 3 shared papers, 2020 · strength 0.32
- Paper Correction to: Musashi2 promotes EGF-induced EMT in pancreatic cancer via ZEB1-ERK/MAPK signaling. DOI 10.1186/s13046-020-01663-2↗
- Paper Musashi2 promotes EGF-induced EMT in pancreatic cancer via ZEB1-ERK/MAPK signaling. DOI 10.1186/s13046-020-1521-4↗
- Paper Calreticulin promotes EMT in pancreatic cancer via mediating Ca2+ dependent acute and chronic endoplasmic reticulum str… DOI 10.1186/s13046-020-01702-y↗
- Qi Dong · 2 shared papers, 2020–2022 · strength 0.29
- Tian Sun · 1 shared paper, 2020 · strength 0.13
- Qingliang Shao · 1 shared paper, 2020 · strength 0.13
- Lei Zhou · 1 shared paper, 2020 · strength 0.11
- Jianping Zhou · 1 shared paper, 2020 · strength 0.11
How to reach this person
A chain of introductions through people who have published, run trials or held grants together (warm_path@1: fewest links first, then the strongest). Built from public records only; no contact details are kept.