Publications

Jun He, PhD

Contact

Name: Jun He, PhD
Position: Assistant Professor

1020 Locust Street
336 JAH
Philadelphia, PA 19107

Telephone: 215-503-6148

Laboratory

Telephone: 215-503-6159

Highlighted Publications

Shi ZM, Wang L, Shen H, Jiang CF, Ge X, Li DM, He J*, Jiang BH*. Downregulation of miR-218 contributes to epithelial-mesenchymal transition and tumor metastasis in lung cancer by targeting Slug/ZEB2 signaling.  Oncogene, 2017 Feb 13. * Co-corresponding author

These findings highlight an important role of miR-218 in the regulation of EMT-related traits and metastasis of lung cancer in part by modulation of Slug/ZEB2 signaling, and provide a potential therapeutic strategy by targeting miR-218 in NSCLC.    

He J, Yu JJ, Xu Q, Wang L, Zheng J, Liu LZ, Jiang BH. Downregulation of ATG14 by EGR1-MIR152 sensitizes ovarian cancer cells to cisplatin-induced apoptosis by inhibiting cytoprotective autophagy. Autophagy, 2015, 11: 373-84. PMID: 25650716; PMCID: PMC4502709.

This paper showed that miR-152 as a new autophagy-regulating miRNA that is critical in cisplatin-resistance. We identified that ATG14 is a functional target of MIR152 in regulating autophagy inhibition. Furthermore, we found that EGR1 (early growth response 1) regulated the MIR152 gene at the transcriptional level. More importantly, these findings were relevant to clinical cases.

He J, Wang M, Jiang Y, Chen Q, Xu S, Xu Q, Liu LZ, Jiang BH. Chronic arsenic exposure and angiogenesis in human bronchial epithelial cells via ROS/miR-199a-5p/HIF-1α/COX-2 Pathway. Environmental Health Perspectives, 2014, 122: 255-61

This paper demonstrated the critical roles of miR-199a-5p and its downstream targets HIF-1/COX-2 in arsenic-induced tumor growth and angiogenesis.

He J, Xu Q, Jing Y, Agani F, Carpenter R, Qian X, Li Q, Wang XR, Peiper SS, Lu Z, Liu LZ, Jiang BH. Reactive oxygen species regulate ERBB2 and ERBB3 expression via miR-199a/125b and DNA methylation. EMBO Rep., 2012, 13(12): 1116-1122.

Overexpression of ERBB2 or ERBB3 is associated with cancer development and poor prognosis. In this study, we show that reactive oxygen species (ROS) induce both ERBB2 and ERBB3 expression through miR-199a and miR-125b. We also identify that ROS inhibit miR-199a and miR-125b expression through DNA methylation.