ArticleJournal of translational medicine2017
Autocrine parathyroid hormone-like hormone promotes intrahepatic cholangiocarcinoma cell proliferation via increased ERK/JNK-ATF2-cyclinD1 signaling.
Article in Journal of translational medicine, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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Who cites it
19 citing papers in PubMed, 27 citations in OpenAlex.
- Expression profiling of human milk derived exosomal microRNAs and their targets in HIV-1 infected mothers.Scientific reports · 2020Trial
- Single-cell multi-omics analysis reveals drivers of intrahepatic cholangiocarcinoma metastasis.BMC cancer · 2025Article
- [Overexpression of parathyroid hormone-like hormone facilitates hepatocellular carcinoma progression and correlates with adverse outcomes].Nan fang yi ke da xue xue bao = Journal of Southern Medical University · 2025Article
- Silencing PPAP2C inhibits lung adenocarcinoma migration and invasion via the ERK/JNK pathway.Molecular medicine reports · 2025Article
- Review
- PTHrP Regulates Fatty Acid Metabolism via Novel lncRNA in Breast Cancer Initiation and Progression Models.Cancers · 2023Article
- Article
- PRCC reduces the sensitivity of cancer cells to DNA damage by inhibiting JNK and ATM/ATR pathways and results in a poor prognosis in hepatocellular carcinoma.Cell & bioscience · 2021Article
- PTHrP Drives Pancreatic Cancer Growth and Metastasis and Reveals a New Therapeutic Vulnerability.Cancer discovery · 2021Article
- Annexin A7 and JNK knockdown suppress the lymphatic metastasis potential of hepatocellular carcinoma cells: Possible contributions of ATF2 and sequence-related lncRNA NONMMUT114121.1.Translational cancer research · 2021Article
- Research advances of secretory proteins in malignant tumors.Chinese journal of cancer research = Chung-kuo yen cheng yen chiu · 2021Article
- S100A16 suppresses the proliferation, migration and invasion of colorectal cancer cells in part via the JNK/p38 MAPK pathway.Molecular medicine reports · 2021Article
- Sprouty2 Inhibits Migration and Invasion of Fibroblast-Like Synoviocytes in Rheumatoid Arthritis by Down-regulating ATF2 Expression and Phosphorylation.Inflammation · 2021Article
- In Vivo Models for Cholangiocarcinoma-What Can We Learn for Human Disease?International journal of molecular sciences · 2020Review
- Targeting ERK-Hippo Interplay in Cancer Therapy.International journal of molecular sciences · 2020Review
- Article
- Construction of a model to predict the prognosis of patients with cholangiocarcinoma using alternative splicing events.Oncology letters · 2019Article
- Animal models of cholangiocarcinoma.Biochimica et biophysica acta. Molecular basis of disease · 2019Review
- Article
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Authors and funding
21 authors at 3 institutions in 1 country.
Funding
Abstract
BACKGROUND AND
aimsIntrahepatic cholangiocarcinoma (ICC) is an aggressive tumor with a high fatality rate. It was recently found that parathyroid hormone-like hormone (PTHLH) was frequently overexpressed in ICC compared with non-tumor tissue. This study aimed to elucidate the underlying mechanisms of PTHLH in ICC development.
methodsThe CCK-8 assay, colony formation assays, flow cytometry and a xenograft model were used to examine the role of PTHLH in ICC cells proliferation. Immunohistochemistry (IHC) and western blot assays were used to detect target proteins. Luciferase reporter, chromatin immunoprecipitation (ChIP) and DNA pull-down assays were used to verify the transcription regulation of activating transcription factor-2 (ATF2).
resultsPTHLH was significantly upregulated in ICC compared with adjacent and normal tissues. Upregulation of PTHLH indicated a poor pathological differentiation and intrahepatic metastasis. Functional study demonstrated that PTHLH silencing markedly suppressed ICC cells growth, while specific overexpression of PTHLH has the opposite effect. Mechanistically, secreted PTHLH could promote ICC cell growth by activating extracellular signal-related kinase (ERK) and c-Jun N-terminal kinase (JNK) signaling pathways, and subsequently upregulated ATF2 and cyclinD1 expression. Further study found that the promoter activity of PTHLH were negatively regulated by ATF2, indicating that a negative feedback loop exists.
conclusionsOur findings demonstrated that the ICC-secreted PTHLH plays a characteristic growth-promoting role through activating the canonical ERK/JNK-ATF2-cyclinD1 signaling pathways in ICC development. We identified a negative feedback loop formed by ATF2 and PTHLH. In this study, we explored the therapeutic implication for ICC patients.
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