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Jintao He

Researcher at Third Military Medical University

Publications -  15
Citations -  556

Jintao He is an academic researcher from Third Military Medical University. The author has contributed to research in topics: Cancer & HULC. The author has an hindex of 9, co-authored 13 publications receiving 426 citations.

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LncRNA HULC triggers autophagy via stabilizing Sirt1 and attenuates the chemosensitivity of HCC cells

TL;DR: The data reveals that the pathway ‘HULC/USP22/Sirt1/ protective autophagy’ attenuates the sensitivity of HCC cells to chemotherapeutic agents, suggesting that this pathway may be a novel target for developing sensitizing strategy to HCC chemotherapy.
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lncRNA HULC promotes the growth of hepatocellular carcinoma cells via stabilizing COX-2 protein

TL;DR: It is demonstrated for the first time that HULC promoted the growth of HCC cells through elevating COX-2 protein through the role of ubiquitin-specific peptidase 22 (USP22), and the identification of this novel pathway may pave a road for developing new potential anti-HCC strategies.
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Identification of a fluorescent small-molecule enhancer for therapeutic autophagy in colorectal cancer by targeting mitochondrial protein translocase TIM44

TL;DR: A novel NIR small-molecule autophagy-enhancer, IR-58, with mitochondria-targeted imaging and therapy capabilities was developed for CRC treatment and TIM44 was identified for the first time as a potential oncogene, which plays an important role in Autophagy through the TIM44-SOD2-ROS-mTOR pathway.
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Dichloroacetate and metformin synergistically suppress the growth of ovarian cancer cells.

TL;DR: It is found that DCA and Met synergistically inhibited the growth and enhanced the apoptosis of ovarian cancer cells and may pave a way for developing novel strategies for the treatment of ovariancancer based on the combined use ofDCA and metformin.
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AKT-mediated phosphorylation of ATG4B impairs mitochondrial activity and enhances the Warburg effect in hepatocellular carcinoma cells.

TL;DR: The results demonstrate for the first time that the phosphorylation of ATG4B at Ser34 participates in the metabolic reprogramming of HCC cells via repressing mitochondrial function, which possibly results from the Ser34 phosphorylations-induced mitochondrial enrichment of ATg4B and the subsequent inhibition of F1Fo-ATP synthase activity.