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Jin Bai

Researcher at Xuzhou Medical College

Publications -  107
Citations -  2097

Jin Bai is an academic researcher from Xuzhou Medical College. The author has contributed to research in topics: Cancer & Metastasis. The author has an hindex of 21, co-authored 69 publications receiving 1310 citations. Previous affiliations of Jin Bai include Icahn School of Medicine at Mount Sinai.

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LINC00460/DHX9/IGF2BP2 complex promotes colorectal cancer proliferation and metastasis by mediating HMGA1 mRNA stability depending on m6A modification

TL;DR: LINC00460 can serve as a promising predictive biomarker for the diagnosis and prognosis among patients with CRC through interacting with IGF2BP2 and DHX9 and bind to the m6A modified HM GA1 mRNA to enhance the HMGA1 mRNA stability.
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BRG1 is a prognostic marker and potential therapeutic target in human breast cancer.

TL;DR: The Kaplan-Meier survival curves showed that high BRG1 expression is inversely correlated with both overall and disease-specific 5-year patient survival and it was found that knockdown ofBRG1 by RNA interference markedly inhibits cell proliferation and causes cessation of cell cycle.
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p53-mediated autophagic regulation: A prospective strategy for cancer therapy.

TL;DR: The contextual role of autophagy in cancer, which could be switched by p53 status, is expected to be developed into a new anticancer therapeutic approach.
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Rap2B promotes proliferation, migration, and invasion of human breast cancer through calcium-related ERK1/2 signaling pathway

TL;DR: Flow cytometry and Western blot analysis revealed that Rap2B elevates the intracellular calcium level and further promotes extracellular signal-related kinase (ERK) 1/2 phosphorylation, and shed light on Rap2 B as a therapeutic target for breast cancer.
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PTBP3-Mediated Regulation of ZEB1 mRNA Stability Promotes Epithelial-Mesenchymal Transition in Breast Cancer.

TL;DR: It is demonstrated that PTBP3 induces epithelial-mesenchymal transition (EMT) in breast tumor cells and promotes their invasive growth and metastasis and its candidacy as a theranostic target is suggested.