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Proteomic landscape of hydatidiform mole reveals molecular evolution and immune evasion in recurrence
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Mengyan TU1*, Shanshan XU1*, Xinru TU1, Hankai SHI1, Weiguo LU1,2,3, Junfen XU1. Proteomic landscape of hydatidiform mole reveals molecular evolution and immune evasion in recurrence[J]. Journal of Zhejiang University Science B, 1998, -1(-1): .
@article{title="Proteomic landscape of hydatidiform mole reveals molecular evolution and immune evasion in recurrence",
author="Mengyan TU1*, Shanshan XU1*, Xinru TU1, Hankai SHI1, Weiguo LU1,2,3, Junfen XU1",
journal="Journal of Zhejiang University Science B",
volume="-1",
number="-1",
pages="",
year="1998",
publisher="Zhejiang University Press & Springer",
doi="10.1631/jzus.2500753"
}
%0 Journal Article
%T Proteomic landscape of hydatidiform mole reveals molecular evolution and immune evasion in recurrence
%A Mengyan TU1*
%A Shanshan XU1*
%A Xinru TU1
%A Hankai SHI1
%A Weiguo LU1
%A 2
%A 3
%A Junfen XU1
%J Journal of Zhejiang University SCIENCE B
%V -1
%N -1
%P
%@ 1869-1951
%D 1998
%I Zhejiang University Press & Springer
%DOI 10.1631/jzus.2500753
TY - JOUR
T1 - Proteomic landscape of hydatidiform mole reveals molecular evolution and immune evasion in recurrence
A1 - Mengyan TU1*
A1 - Shanshan XU1*
A1 - Xinru TU1
A1 - Hankai SHI1
A1 - Weiguo LU1
A1 - 2
A1 - 3
A1 - Junfen XU1
J0 - Journal of Zhejiang University Science B
VL - -1
IS - -1
SP -
EP -
%@ 1869-1951
Y1 - 1998
PB - Zhejiang University Press & Springer
ER -
DOI - 10.1631/jzus.2500753
Abstract: hydatidiform mole (HM) is a gestational trophoblastic disease causing abnormal trophoblastic proliferation and pregnancy loss, often accompanied by a significant psychological burden. To elucidate the molecular basis and recurrence mechanisms of HM, we performed high-throughput proteomic profiling of FFPE villous tissues from 8 sporadic HM cases (HMS), 6 primary HM from recurrent cases (HMRP), 13 recurrent HM cases (HMR), and 8 normal villus cases (NV). A total of 2,959 differentially expressed proteins were identified, revealing immune dysregulation and metabolic reprogramming in HM. CD55 and ITGAM emerged as central network hubs of HM, while the recurrence-associated signature indicated altered extracellular matrix composition and the suppression of key transcriptional regulators (YAP1, STK3, POU2F1). Proteomic trajectory analysis from HMS to HMR highlighted the persistent downregulation of neutrophil degranulation and the upregulation of the immune checkpoint CD276 (B7-H3). These findings delineate the proteomic evolution and immune landscape of HM, offering molecular insights for recurrence risk assessment and potential targeted therapies for improved clinical management.
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