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Mengyan Xie

Researcher at Nanjing Medical University

Publications -  16
Citations -  1313

Mengyan Xie is an academic researcher from Nanjing Medical University. The author has contributed to research in topics: Cancer & Cancer research. The author has an hindex of 7, co-authored 12 publications receiving 480 citations.

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Role of hypoxia in cancer therapy by regulating the tumor microenvironment

TL;DR: The role of Hypoxia in cancer therapy by regulating the tumor microenvironment (TME) is summarized and the potential of hypoxia-targeted therapy is highlighted to overcome hypoxian-associated resistance in cancer treatment.
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Exosomal circSHKBP1 promotes gastric cancer progression via regulating the miR-582-3p/HUR/VEGF axis and suppressing HSP90 degradation

TL;DR: It is demonstrated that exosomal circSHKBP1 regulates the miR-582-3p/HUR/VEGF pathway, suppresses HSP90 degradation, and promotes GC progression, and is a promising circulating biomarker for GC diagnosis and prognosis and an exceptional candidate for further therapeutic exploration.
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The Biogenesis and Functions of piRNAs in Human Diseases.

TL;DR: This review illustrates piRNA biogenesis, mechanisms behind piRNA-mediated gene regulation, and changes of piRNAs in different diseases, especially in cancers.
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Silencing of circRACGAP1 sensitizes gastric cancer cells to apatinib via modulating autophagy by targeting miR-3657 and ATG7.

TL;DR: Findings provided the first evidence that the circRACGAP1-miR-3657-ATG7 axis mediates a novel regulatory pathway critical for the regulation of apatinib sensitivity in GC, and specific blockage of circRAP1 may be a potential therapeutic strategy to reduce the toxicities ofApatinib and enhance its therapeutic effect in human GC.
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MiR-598 Suppresses Invasion and Migration by Negative Regulation of Derlin-1 and Epithelial-Mesenchymal Transition in Non-Small Cell Lung Cancer.

TL;DR: Findings for the first time revealed that miR-598, as a tumor suppressor, negatively regulate DERL1 and EMT to suppress the invasion and migration in NSCLC, thereby putatively serving as a novel therapeutic target forNSCLC clinical treatment.