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Linlin Zhang

Researcher at Xi'an Jiaotong University

Publications -  34
Citations -  1178

Linlin Zhang is an academic researcher from Xi'an Jiaotong University. The author has contributed to research in topics: LNCaP & Prostate cancer. The author has an hindex of 15, co-authored 34 publications receiving 1036 citations. Previous affiliations of Linlin Zhang include Chinese Ministry of Education & Beijing Jiaotong University.

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Role of Wnt/β‐catenin signaling pathway in epithelial‐mesenchymal transition of human prostate cancer induced by hypoxia‐inducible factor‐1α

TL;DR: This study aims to determine whether the signal of HIF‐1α for inducing prostate cancer cells to undergo EMT might possibly pass through the Wnt/β‐catenin pathway.
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Silibinin inhibits prostate cancer invasion, motility and migration by suppressing vimentin and MMP-2 expression.

TL;DR: This study shows that silibinin could inhibit the invasion, motility and migration of ARCaPM cells via down-regulation of vimentin and MMP-2 and therefore may be a promising agent against prostate cancer bone metastasis.
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Genistein inhibits the stemness properties of prostate cancer cells through targeting Hedgehog-Gli1 pathway.

TL;DR: It is found that tumorsphere formation and colony formation of Pca cells were noticeably suppressed in the presence of genistein, demonstrating that genisteIn may be a dietary phytochemical with potential to target prostate CSCs.
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Silibinin inhibits β-catenin/ZEB1 signaling and suppresses bladder cancer metastasis via dual-blocking epithelial–mesenchymal transition and stemness

TL;DR: A novel mechanism for silibinin targeting bladder cancer metastasis is revealed, in which inactivation of β-catenin/ZEB1 signaling by silib inin leads to dual-block of EMT and stemness.
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Silibinin inhibits cell growth and induces apoptosis by caspase activation, down-regulating survivin and blocking EGFR-ERK activation in renal cell carcinoma.

TL;DR: The results indicated that silibinin effectively inhibits the renal cancer carcinoma Caki-1 cell proliferation and induces apoptosis through inhibiting the activation of EGFR and ERK and the expression of survivin, up-regulating theexpression of p53 and triggering the cascades of caspase pathways.