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Jun He

Researcher at Tianjin University of Traditional Chinese Medicine

Publications -  99
Citations -  2805

Jun He is an academic researcher from Tianjin University of Traditional Chinese Medicine. The author has contributed to research in topics: High-performance liquid chromatography & Cancer. The author has an hindex of 24, co-authored 96 publications receiving 2090 citations. Previous affiliations of Jun He include Thomas Jefferson University & Nanjing Medical University.

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A regulatory circuit of miR-148a/152 and DNMT1 in modulating cell transformation and tumor angiogenesis through IGF-IR and IRS1

TL;DR: It is demonstrated that IGF-IR and IRS1, often overexpressed in BC, are two novel targets of miR-148a/152, and that restoration of microRNAs expression may provide a strategy for therapeutic application to treat BC patients.
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MicroRNA-143 inhibits tumor growth and angiogenesis and sensitizes chemosensitivity to oxaliplatin in colorectal cancers.

TL;DR: Levels in human blood and tumor tissues are associated with CRC cancer occurrence, metastasis and drug resistance, and miR-143 levels may be used as a new diagnostic marker and therapeutic target for CRC in the future.
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Downregulation of ATG14 by EGR1-MIR152 sensitizes ovarian cancer cells to cisplatin-induced apoptosis by inhibiting cyto-protective autophagy

TL;DR: MIR152 is reported as a new autophagy-regulating miRNA that plays a role in cisplatin-resistance and it is found that EGR1 (early growth response 1) regulated the MIR152 gene at the transcriptional level.
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Upregulated long non-coding RNA AGAP2-AS1 represses LATS2 and KLF2 expression through interacting with EZH2 and LSD1 in non-small-cell lung cancer cells

TL;DR: Analysis of lncRNA expression in human NSCLC samples by using microarray data from Gene Expression Omnibus indicates that AGAP2-AS1 may act as an oncogene by repressing tumor-suppressor LATS2 and KLF2 transcription.
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Reactive oxygen species regulate ERBB2 and ERBB3 expression via miR‐199a/125b and DNA methylation

TL;DR: It is shown that reactive oxygen species (ROS) induce both ERBB2 and ERBB3 expression in vitro and in vivo, and that ERBB 2 and ER BB3 expression is regulated by ROS via miR‐199a and miR-125b downregulation and DNA hypermethylation.