Jinghu He

Dr. Jinghu He


Research Focus & Metrics

Academic Career Length

4Years (2023-Present)

(Calculated once Scilit publication data is synced: current year − year of first publication + 1)

Representative Publications

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14 September 2023 in Journal of Translational Medicine
Verified
Journal Article
Open access
PDF file
SYShaojun Yu
Shaojun Yu
WDWeixing Dai
Weixing Dai
SZSenlin Zhao
Senlin Zhao
YYYongzhi Yang
Yongzhi Yang
YXYe Xu
Ye Xu
DSDebing Shi
Debing Shi
Colorectal cancer (CRC) has become a global health problem which has almost highest morbidity and mortality in all types of cancers. This study aimed to uncover the biological functions and underlying mechanism of MCM8 in the development and progression of CRC. The expression level of MCM8 was found to be upregulated in CRC tissues and significantly associated with tumor grade and patients’ survival. Knocking down MCM8 expression in CRC cells could restrain cell growth and cell motility while promoting cell apoptosis in vitro, as well as inhibit tumor growth in xenograft mice model. Based on the RNA screening performing on CRC cells with or without MCM8 knockdown and the following IPA analysis, CHSY1 was identified as a potential target of MCM8 in CRC, whose expression was also found to be higher in tumor tissues than in normal tissues. Moreover, it was demonstrated that MCM8 may regulate the expression of CHSY1 through affecting its NEDD4-mediated ubiquitination, both of which synergistically execute tumor promotion effects on CRC. In conclusion, the outcomes of our study showed the first evidence that MCM8 act as a tumor promotor in CRC, and may be a promising therapeutic target of CRC treatment.

24 April 2025 in Brain Research
Verified
Journal Article
Closed access
JHJinghu He
Jinghu He
ZGZhiyuan Gao
Zhiyuan Gao
XLXilian Li
Xilian Li
LZLong Zhao
Long Zhao
XTXue Tian
Xue Tian
BIAO GAOBIAO GAO
BIAO GAO

15 June 2025 in Molecular Medicine
Verified
Journal Article
Open access
PDF file
LHLiyong Huang
Liyong Huang
YTYixin Tong
Yixin Tong
XLXu Li
Xu Li
WWWei Wang
Wei Wang
ZWZhen Wang
Zhen Wang
JHJinghu He
Jinghu He
Colorectal cancer (CRC) remains a significant health challenge globally, demanding a comprehensive understanding of its molecular underpinnings for effective management. In this study, we investigated the role of Aldolase C (ALDOC), a glycolytic enzyme, in CRC pathogenesis. Transcriptomic analysis of CRC tissues from The Cancer Genome Atlas (TCGA) revealed a substantial upregulation of ALDOC, correlating with adverse clinical outcomes. Immunohistochemical (IHC) staining of locally collected patient-derived tissues corroborated these findings, demonstrating elevated ALDOC expression in tumor tissues, particularly in advanced stages. Functional studies elucidated the regulatory role of ALDOC in CRC cell phenotypes. ALDOC knockdown significantly inhibited cell proliferation, induced apoptosis, arrested cell cycle progression, and suppressed cell migration in vitro. Moreover, in vivo studies using xenograft models confirmed that ALDOC knockdown attenuated tumor growth. Mechanistically, ALDOC was found to interact with hypoxia-inducible factor 1 alpha (HIF1A) and enhance its transcriptional activity on phosphoglycerate kinase 1 (PGK1), a key glycolytic enzyme. Dual-luciferase reporter assays and chromatin immunoprecipitation experiments validated the ALDOC-mediated transcriptional activation of PGK1. Further functional rescue experiments revealed a synergistic interplay between ALDOC and PGK1 in regulating CRC cell phenotypes. Additionally, ALDOC was implicated in promoting aerobic glycolysis in CRC cells, potentially through PGK1 regulation. Collectively, our findings unveil ALDOC as a critical regulator of CRC pathogenesis, offering insights into its potential as a therapeutic target and highlighting the ALDOC/PGK1 axis as a promising avenue for further investigation in CRC.

1 April 2025 in Science Progress
Verified
Journal Article
Open access
LZLaicheng Zhu
Laicheng Zhu
FZFei Zhao
Fei Zhao
WLWenjing Liu
Wenjing Liu
ABAnna Bao
Anna Bao
GWGang Wang
Gang Wang
BIAO GAOBIAO GAO
BIAO GAO
Abdominal cocoon syndrome is a rare cause of small-bowel obstruction characterized by a fibro-collagenous membrane that surrounds the intestine. Here, we report a documented case in which extensive fibrous membrane stripping was combined with intraoperative placement of a transnasal intestinal decompression tube, achieving rapid recovery and durable patency. We describe a patient in his 60s with intermittent abdominal distension, colicky pain, and complete arrest of flatus and stool. Contrast-enhanced computed tomography revealed clustered jejuno-ileal loops enveloped by soft tissue density, raising suspicion of encapsulating peritonitis. Diagnostic laparoscopy identified a thick, whitish membrane that covered the stomach, whole small intestine, colon, and mesentery; after extensive adhesiolysis, the operation was converted to laparotomy for complete membrane stripping and placement of a transnasal intestinal decompression tube. Histology demonstrated proliferative fibrous tissue without IgG4-positive plasma cell infiltration, excluding IgG4-related disease. The patient resumed oral intake on postoperative day 2, was discharged on day 22, and remained asymptomatic with patent bowel loops on 3-month imaging. This case underscores the importance of cross-sectional imaging for early suspicion, supports a strategy of laparoscopic exploration followed by open decortication when necessary, and suggests that intraoperative nasointestinal tube placement may mitigate early recurrent obstruction.