I received my Bachelor’s degree in Clinical Medicine from Fudan University in 2019 and
began my postgraduate studies in Plastic and Reconstructive Surgery at Shanghai Ninth
People’s Hospital, affiliated to Shanghai Jiao Tong University School of Medicine. My
research interests lie in skin wound healing and pathological scars, and I am actively
involved in both laboratory research and clinical trials. My academic work has been
published in journals such as Molecular Therapy, the Journal of Investigative Dermatology.
Additionally, I hold a medical practitioner license in China and have gained two years of
experience treating outpatients under the guidance of Professor Min Yao. I am dedicated
to advancing the field through innovative research and clinical practice.
Education
2014.9-2019.6 Fudan University Bachelor of Clinical Medicine
2019.9-2022.6 Shanghai Jiao Tong University Master of Surgery (PRS)
2022.9-present Shanghai Jiao Tong University Doctor of Surgery (PRS)
Publications (First author or co-first author)
Gu, S., Huang, X., Luo, S., Liu, Y., Khoong, Y., Liang, H., Tu, L., Xu, R., Yang, E., Zhao,
Y., Yao, M., Zan, T. Targeting the nuclear long noncoding transcript LSP1P5 abrogates
extracellular matrix deposition by trans-upregulating CEBPA in keloids. Molecular therapy.
2024;32(6):1984-1999. doi:10.1016/j.ymthe.2024.03.031
Gu, S., Khoong, Y., Gao, Y., Li, H., Gu, B., Xie, F., Huang, X., Zan, T. Identification of
the optimal predictive cutoff value for expanded flap viability using Indocyanine Green
Angiography: A prospective study. Burns & trauma. 2024;12:tkae019.
doi:10.1093/burnst/tkae019
Tu, L., Gu, S., Xu, R., Yang, E., Huang, X., Liang, H., Luo, S., Li, H., Zhao, Y., Zan, T.
ALKBH3-Mediated M1A Demethylation of METTL3 Endows Pathological Fibrosis:
Interplay Between M1A and M6A RNA Methylation. Advanced science. Advance online
publication.
Huang, X., Gu, S., Liu, C., Zhang, L., Zhang, Z., Zhao, Y., Khoong, Y., Li, H., Gao, Y.,
Liu, Y., Wang, Z., Zhao, D., Li, Q., Zan, T. (2022). CD39+ Fibroblasts Enhance
Myofibroblast Activation by Promoting IL-11 Secretion in Hypertrophic Scars. The
Journal of investigative dermatology. 2022; 142(4), 1065–1076.e19.
doi:10.1016/j.jid.2021.07.181
Gu, S., Huang, X., Xu, X., Liu, Y., Khoong, Y., Zhang, Z., Li, H., Gao, Y., Zan, T.
Inhibition of CUB and sushi multiple domains 1 (CSMD1) expression by miRNA-190a-
3p enhances hypertrophic scar-derived fibroblast migration in vitro. BMC genomics.
2021;22(1):613. doi:10.1186/s12864-021-07920-8
Gu, S., Khoong, Y., Huang, X., Zan, T. Facial cleft? The first case of manitoba-oculotricho-
anal syndrome with novel mutations in China: a case report. BMC pediatrics.
2021;21(1):46. doi:10.1186/s12887-021-02506-5
Xu, X., Gu, S., Huang, X., Ren, J., Gu, Y., Wei, C., Lian, X., Li, H., Gao, Y., Jin, R., Gu,
B., Zan, T., Wang, Z. The role of macrophages in the formation of hypertrophic scars and
keloids. Burns & trauma. 2020;8:tkaa006. doi:10.1093/burnst/tkaa006
Huang, X., Li, H., Gu, S., Gao, Y., Khoong, Y., Liu, Y., Luo, S., Gu, B., Li, Q., Zan, T.
Intraoperative Indocyanine Green Angiography Facilitates Flap Fenestration and Facial
Organ Fabrication in Total Facial Restoration. Plastic and reconstructive surgery.
2024;153(6):1416-1424. doi:10.1097/PRS.0000000000010891.
Wei CJ, Gu SC, Ren JY, et al. The impact of host immune cells on the development of
neurofibromatosis type 1: The abnormal immune system provides an immune
microenvironment for tumorigenesis. Neurooncol Adv. 2019;1(1):vdz037.
doi:10.1093/noajnl/vdz037
Honors and Awards
2024, the member of American Society of Gene & Cell Therapy (ASGCT)
2023, National Natural Science Foundation, Lindau Scholar
2021, National scholarship
2019, Outstanding graduate of Fudan University
Academic activities
2024, SPIE Photonics West Event, oral presentation, San Francisco, CA, US
2023, 72nd Lindau Nobel Laureate Meeting, attendance, Lindau, Germany
2023, 20th National Academic Conference of Chinese Medical Association Plastic Surgery
Branch, oral presentation, Nanchang, China
2019.4-2019.5, The Royal Melbourne Hospital, International medical student, Melbourne,
Australia
Research Interest
Fibroblast subtypes in hypertrophic scars
Epigenetic mechanisms in skin wound healing and pathological scars
Application of indocyanine green angiography (ICGA) in reconstructive surgery
Research Skills
Primary cell extraction and culture
Cell functional assays (CCK8, Edu, transwell, scratch, Tunel)
Nuclear-cytoplasmic separation
RNA interference (siRNA, shRNA, ASO)
Lenti-virus packaging and transfection
RNA extraction, reverse transcription and Polymerase Chain Reaction (PCR)
Fluorescence In Situ Hybridization (FISH)
Western Blot (WB), Immunohistochemistry (IHC) and Immunofluorescence (IF)
RNA Immunoprecipitation (RIP) and Chromatin Immunoprecipitation (ChIP)
Formaldehyde-Assisted Isolation of Regulatory Elements (FAIRE)
Animal models of skin wound, fibrosis and pathological scars
Languages
Chinese, English, Japanese
Abstract submitted for the 5th International Keloid Symposium
Title: Targeting the nuclear long noncoding transcript LSP1P5 abrogates extracellular matrix deposition by trans-upregulating CEBPA in keloids
AUTHORS: Shuchen Gu, Xin Huang, Shenying Luo, Yunhan Liu, Yimin Khoong, Liying Tu, Yixuan Zhao, Min Yao, Tao Zan
AUTHORS’ AFFILIATIONS:
Department of Plastic and Reconstructive Surgery, Shanghai Ninth People’s Hospital, Shanghai Jiao Tong University School of Medicine
Background:
The function of long noncoding RNA (lncRNA)-mediated ECM remodeling during the pathogenesis of keloids is unclear. We identified a human specific long noncoding transcript, namely, lymphocyte-specific protein 1 pseudogene 5 (LSP1P5), that modulates ECM component deposition in keloids.
Methods:
Four pairs of typical keloid tissues and adjacent normal skin tissues were collected. RNA sequencing was performed to identify key lncRNAs in keloids, with LSP1P5 being the most significantly upregulated transcript. Subcellular localization of LSP1P5 was investigated using RNA fluorescence in situ hybridization and cellular fractionation assay. Two antisense oligonucleotide sequences were employed to knock down LSP1P5 in keloid derived fibroblasts (KDFs), keloid in vitro and in vivo models. Levels of myofibroblast activation and expression levels of extracellular matrix (ECM)-related proteins were assessed in both LSP1P5 knockdown groups and their respective control groups. RNA sequencing was used to identify differentially expressed genes following LSP1P5 knockdown, with GO analysis identifying enriched biological functions. IPA analysis was conducted to determine upstream regulators, identifying key transcription factors that may play a role. Mechanistic interactions between LSP1P5 and these transcription factors were explored using techniques such as RNA immunoprecipitation, FAIRE, ChIP, and CUT&Tag.
Results:
Nuclear LSP1P5 is upregulated in both keloid tissue and fibroblasts. Functional analysis revealed that LSP1P5 is necessary to maintain high levels of ECM components, including collagen 1 (COL1), collagen 3 (COL3) and fibronectin 1 (FN1), both in vitro and in vivo. CEBPA was identified as a downstream candidate of LSP1P5 and shown to exhibit antifibrotic effects on the skin. After LSP1P5 knockdown, CEBPA was significantly upregulated. Mechanistically, LSP1P5 hijacks polycomb repressive complex 2 (PRC2) to the promoter of CEBPA by interacting with Suppressor of Zeste 12 (SUZ12), catalyzing the trimethylation of lysine 27 on histone 3 (H3K27me3) of CEBPA, and thereby influencing the chromosomal opening status which results in the silencing of CEBPA.
Conclusion:
LSP1P5 recruits PRC2 to the CEBPA promoter region, mediating H3K27me3 and regulating chromatin accessibility to silence CEBPA, thereby promoting matrix deposition in keloids.
