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Updated: Jul 19, 2026

Conditional Reprogramming of Pediatric Human Esophageal Epithelial Cells for Use in Tissue Engineering and Disease Investigation
Published on: March 22, 2017
Heterogeneous nuclear ribonucleoprotein C deficiency compromises extracellular matrix-receptor interaction and
Gangfeng Ding1, Jiayao He1, Yichao Chen1
1The First Affiliated Hospital of Wenzhou Medical University, Wenzhou Medical University, Wenzhou, China.
Abstract:
Esophageal cancer (EC) is a highly aggressive malignancy associated with high rates of recurrence and metastasis, and the five-year survival rate remains only 20-30%. N6-methyladenosine (m6A), the most abundant mRNA modification, plays a pivotal role in regulating gene expression and disease pathogenesis. As an m6A "reader," heterogeneous nuclear ribonucleoprotein C (HNRNPC) binds RNA through its recognition motif and has been shown to contribute to the progression of several cancers, including colorectal, breast, and non-small cell lung cancer. However, its function and mechanism in EC remain unclear. In this study, we demonstrated that HNRNPC was upregulated in EC and correlated with poor prognosis, based on analyses of public databases and a clinical cohort. Using the xenograft mouse model, we found that HNRNPC knockdown suppressed EC tumor growth in vivo. Interestingly, mechanistic studies revealed that HNRNPC depletion promoted cell apoptosis without affecting proliferation, thereby inhibiting tumor growth. At the molecular level, HNRNPC deficiency selectively influenced transcripts with complex structures, such as CD44, OLFML2A, and PCSK6, and subsequently disrupted extracellular matrix-receptor interactions, leading to impeded tumor progression.
Insights
Heterogeneous nuclear ribonucleoprotein C (HNRNPC) is upregulated in esophageal cancer (EC), driving tumor growth by inhibiting apoptosis. Suppressing HNRNPC shows promise for treating this aggressive cancer.
Area of Science:
- Oncology
- Molecular Biology
- Epigenetics
Background:
- Esophageal cancer (EC) is aggressive with poor survival rates.
- N6-methyladenosine (m6A) modification regulates gene expression and disease.
- HNRNPC, an m6A reader, is implicated in various cancers but its role in EC is unknown.
Purpose of the Study:
- To investigate the function and mechanism of HNRNPC in esophageal cancer.
- To determine the correlation between HNRNPC expression and EC prognosis.
Main Methods:
- Analysis of public databases and a clinical cohort.
- In vivo studies using a xenograft mouse model.
- Molecular analyses of gene expression and cellular processes.
Main Results:
- HNRNPC was upregulated in EC and associated with poor prognosis.
- HNRNPC knockdown suppressed tumor growth in vivo by promoting apoptosis.
- HNRNPC deficiency affected complex transcripts and disrupted extracellular matrix-receptor interactions.
Conclusions:
- HNRNPC promotes esophageal cancer progression.
- Targeting HNRNPC may be a potential therapeutic strategy for EC.
- HNRNPC influences EC tumorigenesis through modulation of specific gene networks.
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