---
title: "MIR100HG drives HCC tumorigenic traits via p38/MAPK and AKT signaling in an oxygen-dependent manner"
id: "pubmed-42698010"
canonical_url: "https://medichelpline.com/clinical-feed/pubmed-42698010"
content_type: "clinical_feed_article"
specialty: "Oncology"
source_name: "PubMed / NCBI"
source_url: "https://pubmed.ncbi.nlm.nih.gov/42698010/"
doi: "10.1007/s10142-026-02033-5"
published_at: "2026-09-05T00:00:00.000Z"
evidence_level: "Journal Article"
license: "CC-BY-NC-4.0 / Informational Use"
---
# MIR100HG drives HCC tumorigenic traits via p38/MAPK and AKT signaling in an oxygen-dependent manner
## Provenance & Clinical Metadata
- **Canonical URL:** https://medichelpline.com/clinical-feed/pubmed-42698010
- **Specialty:** [Oncology](https://medichelpline.com/clinical-feed/oncology.md)
- **Primary Source:** PubMed / NCBI
- **Source URL:** [Original Journal Publication](https://pubmed.ncbi.nlm.nih.gov/42698010/)
- **DOI:** [10.1007/s10142-026-02033-5](https://doi.org/10.1007%2Fs10142-026-02033-5)
- **Published At:** 2026-09-05T00:00:00.000Z
- **Evidence Rating:** Journal Article
## Executive GIST (TL;DR)
- Hepatocellular carcinoma (HCC) progression is promoted by hypoxic tumor microenvironments that alter signaling and therapeutic responses. - The long non-coding RNA **MIR100HG** was evaluated for expression and function in epithelial-like Hep3B and mesenchymal-like SNU-398 HCC cell lines and in non-tumor Clone-9 hepatocytes. - Gain- and loss-of-function experiments (overexpression and silencing) were used to assess effects on proliferation, clonogenicity, migration, invasion, and apoptosis under both normoxic and hypoxia-mimicking conditions. - **MIR100HG overexpression** increased cell proliferation, colony formation, migration, and invasion; **MIR100HG silencing** suppressed these tumorigenic phenotypes and increased apoptotic cell death. - Mechanistically, MIR100HG promoted oncogenic signaling through activation (phosphorylation) of **p38/MAPK** and **AKT** under normoxic conditions; MIR100HG depletion reduced phosphorylation of these proteins. - Under hypoxia-mimicking conditions, the MIR100HG-associated activation of p38/MAPK and AKT observed in normoxia was not preserved, indicating a context-dependent signaling response. - Expression of AKT-associated regulatory genes such as **GAS6** and **PTEN** was reversed under hypoxia-mimicking conditions compared with normoxia, reflecting hypoxia-driven remodeling of downstream pathways. - The study identifies MIR100HG as a **hypoxia-associated oncogenic regulator** in HCC, supporting its potential as a biomarker and therapeutic target; details on in vivo validation and clinical correlation were not reported in the source abstract. - The authors declared no competing interests and stated that ethical approval was not required because no animal or human subjects were used.
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Affiliations Expand ### Affiliations * 1 Faculty of Science and Literature, Department of Molecular Biology and Genetics, Balikesir University, Balıkesir, Turkey. * 2 Institute of Oncology, Department of Translational Oncology, Dokuz Eylul University, Izmir, Turkey. * 3 Faculty of Science and Literature, Department of Molecular Biology and Genetics, Balikesir University, Balıkesir, Turkey. fkockar@balikesir.edu.tr. * PMID: **42698010** * DOI: [ 10.1007/s10142-026-02033-5 ](https://doi.org/10.1007/s10142-026-02033-5) Item in Clipboard # Context-dependent effects of MIR100HG on tumorigenic phenotypes and p38/MAPK-AKT signaling in hepatocellular carcinoma Esra Tokay et al. Funct Integr Genomics. 2026. Show details Display options Display options Format Abstract PubMed PMID Funct Integr Genomics Actions * [ Search in PubMed ](https://pubmed.ncbi.nlm.nih.gov/?term=%22Funct+Integr+Genomics%22%5Bjour%5D&sort=date&sort_order=desc) * [ Search in NLM Catalog ](https://www.ncbi.nlm.nih.gov/nlmcatalog?term=%22Funct+Integr+Genomics%22%5BTitle+Abbreviation%5D) * [ Add to Search ](https://pubmed.ncbi.nlm.nih.gov/42698010/) . 2026 Sep 5;26(1):249. doi: 10.1007/s10142-026-02033-5. ### Authors [Esra Tokay](https://pubmed.ncbi.nlm.nih.gov/?term=Tokay+E&cauthor_id=42698010)[ 1 ](https://pubmed.ncbi.nlm.nih.gov/42698010/#short-view-affiliation-1 "Faculty of Science and Literature, Department of Molecular Biology and Genetics, Balikesir University, Balıkesir, Turkey."), [Sevin Avsar Koc](https://pubmed.ncbi.nlm.nih.gov/?term=Koc+SA&cauthor_id=42698010)[ 1 ](https://pubmed.ncbi.nlm.nih.gov/42698010/#short-view-affiliation-1 "Faculty of Science and Literature, Department of Molecular Biology and Genetics, Balikesir University, Balıkesir, Turkey."), [Aylin Turkoglu Dulger](https://pubmed.ncbi.nlm.nih.gov/?term=Dulger+AT&cauthor_id=42698010)[ 1 ](https://pubmed.ncbi.nlm.nih.gov/42698010/#short-view-affiliation-1 "Faculty of Science and Literature, Department of Molecular Biology and Genetics, Balikesir University, Balıkesir, Turkey."), [Rümeysa Alacam](https://pubmed.ncbi.nlm.nih.gov/?term=Alacam+R&cauthor_id=42698010)[ 1 ](https://pubmed.ncbi.nlm.nih.gov/42698010/#short-view-affiliation-1 "Faculty of Science and Literature, Department of Molecular Biology and Genetics, Balikesir University, Balıkesir, Turkey."), [Nelin Hacioglu](https://pubmed.ncbi.nlm.nih.gov/?term=Hacioglu+N&cauthor_id=42698010)[ 1 ](https://pubmed.ncbi.nlm.nih.gov/42698010/#short-view-affiliation-1 "Faculty of Science and Literature, Department of Molecular Biology and Genetics, Balikesir University, Balıkesir, Turkey."), [Meltem Alper](https://pubmed.ncbi.nlm.nih.gov/?term=Alper+M&cauthor_id=42698010)[ 2 ](https://pubmed.ncbi.nlm.nih.gov/42698010/#short-view-affiliation-2 "Institute of Oncology, Department of Translational Oncology, Dokuz Eylul University, Izmir, Turkey."), [Feray Kockar](https://pubmed.ncbi.nlm.nih.gov/?term=Kockar+F&cauthor_id=42698010)[ 3 ](https://pubmed.ncbi.nlm.nih.gov/42698010/#short-view-affiliation-3 "Faculty of Science and Literature, Department of Molecular Biology and Genetics, Balikesir University, Balıkesir, Turkey. fkockar@balikesir.edu.tr.") ### Affiliations * 1 Faculty of Science and Literature, Department of Molecular Biology and Genetics, Balikesir University, Balıkesir, Turkey. * 2 Institute of Oncology, Department of Translational Oncology, Dokuz Eylul University, Izmir, Turkey. * 3 Faculty of Science and Literature, Department of Molecular Biology and Genetics, Balikesir University, Balıkesir, Turkey. fkockar@balikesir.edu.tr. * PMID: **42698010** * DOI: [ 10.1007/s10142-026-02033-5 ](https://doi.org/10.1007/s10142-026-02033-5) Item in Clipboard Cite Display options Display options Format Abstract PubMed PMID ## Abstract Hepatocellular carcinoma (HCC) is one of the leading causes of cancer-related mortality worldwide and is characterized by a hypoxic tumor microenvironment that promotes tumor progression, cellular adaptation, and therapeutic resistance. Increasing evidence indicates that long non-coding RNAs (lncRNAs) play critical roles in regulating tumor-associated signaling networks; however, the contribution of MIR100HG to hepatocellular carcinoma progression, particularly under hypoxic conditions, remains insufficiently understood. In this study, we investigated the expression pattern and functional significance of MIR100HG in hepatocellular carcinoma using epithelial-like Hep3B and mesenchymal-like SNU-398 cells, together with non-tumor hepatocytes (Clone-9). Gain- and loss-of-function approaches were employed to evaluate the impact of MIR100HG on tumor-associated cellular phenotypes under both normoxic and hypoxic conditions. Functional assays demonstrated that MIR100HG overexpression significantly enhanced cell proliferation, clonogenic potential, migration, and invasion, whereas MIR100HG silencing markedly suppressed these tumorigenic properties and increased apoptotic cell death. Mechanistic analyses revealed that MIR100HG promotes oncogenic signaling through the p38/MAPK and AKT pathways under normoxic conditions, whereas MIR100HG depletion reduced the phosphorylation of these key signaling proteins. Notably, additional pathway analyses under hypoxia-mimicking conditions revealed a distinct signaling response, in which the MIR100HG-associated activation of p38/MAPK and AKT observed under normoxia was not maintained. Moreover, the expression patterns of AKT-associated regulatory genes, including GAS6 and PTEN, were reversed under hypoxia-mimicking conditions. These findings suggest that the effects of MIR100HG on oncogenic signaling are highly dependent on the cellular oxygenation context and that hypoxia reshapes the downstream signaling consequences of MIR100HG expression in HCC cells. Collectively, our findings identify MIR100HG as a hypoxia-associated oncogenic regulator that enhances tumorigenic phenotypes and promotes survival signaling in hepatocellular carcinoma. These results highlight MIR100HG as a potential biomarker and therapeutic target in liver cancer and provide new insights into the molecular mechanisms underlying hypoxia-driven tumor progression. **Keywords:** HCC; Hypoxia; Long non-coding RNA; MIR100HG; Over expression; Pathway; Silencing. © 2026. The Author(s), under exclusive licence to Springer-Verlag GmbH Germany, part of Springer Nature. [PubMed Disclaimer](https://pubmed.ncbi.nlm.nih.gov/disclaimer/) ## Conflict of interest statement Declarations. Competing interests: The authors declare no competing interests. Ethics Approval: This article does not contain research in which animals or humans were used, so ethical approval was not required for this study. ## References 1. 1. Abdel-Rahman O (2013) Systemic therapy for hepatocellular carcinoma (HCC): from bench to bedside. J Egypt Natl Cancer Inst 25(4):165–171. - [DOI](https://doi.org/10.1016/j.jnci.2013.08.002) 2. 1. Alper M, Sav KALFAY, Eroğlu Fnur, K. P. A. S. P. A. L., Köçkar F (2025) TNF-α-Induced Upregulation of ADAMTS-8 Expression in SW480 Cells: Implications for Intracellular Signaling Pathways and Transcription Factor Activity. Cell Biochem Biophys 2025 84:1(1):927–942. . 84 - [DOI](https://doi.org/10.1007/s12013-025-01911-2) 3. 1. Alper M, Sav FN, Keleş Y, Eroğlu KP, Keskin SD, Köçkar F (2025) STAT-3, ELK-1, and c- Jun contributes IL-6 mediated ADAMTS-8 upregulation in colorectal cancer. Mol Biol Rep 52(1). 4. 1. Altuntaş C, Alper M, Keleş Y, Sav FN, Köçkar F (2023) Hypoxic regulation of ADAMTS-2 and – 3 (a disintegrin and matrix metalloproteinase with thrombospondin motifs 2 and 3) procollagen N proteinases by HIF-1α in endothelial cells. Mol Cell Biochem 478(5):1151–1160. - [DOI](https://doi.org/10.1007/s11010-022-04549-3) - [PubMed](https://pubmed.ncbi.nlm.nih.gov/36241950/) 5. 1. Bevilacqua V, Gioia U, Di Carlo V, Tortorelli AF, Colombo T, Bozzoni I, Laneve P, Caffarelli E (2015) Identification of linc-NeD125, a novel long non coding RNA that hosts miR-125b-1 and negatively controls proliferation of human neuroblastoma cells. Taylor Francis 12(12):1323–1337. - [DOI](https://doi.org/10.1080/15476286.2015.1096488) Show all 45 references ## MeSH terms * Carcinogenesis / genetics Actions * [ Search in PubMed ](https://pubmed.ncbi.nlm.nih.gov/?term=%22Carcinogenesis%2Fgenetics%22%5BMeSH%5D&sort=date&sort_order=desc) * [ Search in MeSH ](https://www.ncbi.nlm.nih.gov/mesh?term=Carcinogenesis) * [ Add to Search ](https://pubmed.ncbi.nlm.nih.gov/42698010/) * Carcinoma, Hepatocellular* / genetics Actions * [ Search in PubMed ](https://pubmed.ncbi.nlm.nih.gov/?term=%22Carcinoma%2C+Hepatocellular%2Fgenetics%22%5BMAJR%5D&sort=date&sort_order=desc) * [ Search in MeSH ](https://www.ncbi.nlm.nih.gov/mesh?term=Carcinoma%2C+Hepatocellular) * [ Add to Search ](https://pubmed.ncbi.nlm.nih.gov/42698010/) * Carcinoma, Hepatocellular* / metabolism Actions * [ Search in PubMed ](https://pubmed.ncbi.nlm.nih.gov/?term=%22Carcinoma%2C+Hepatocellular%2Fmetabolism%22%5BMAJR%5D&sort=date&sort_order=desc) * [ Search in MeSH ](https://www.ncbi.nlm.nih.gov/mesh?term=Carcinoma%2C+Hepatocellular) * [ Add to Search ](https://pubmed.ncbi.nlm.nih.gov/42698010/) * Carcinoma, Hepatocellular* / pathology Actions * [ Search in PubMed ](https://pubmed.ncbi.nlm.nih.gov/?term=%22Carcinoma%2C+Hepatocellular%2Fpathology%22%5BMAJR%5D&sort=date&sort_order=desc) * [ Search in MeSH ](https://www.ncbi.nlm.nih.gov/mesh?term=Carcinoma%2C+Hepatocellular) * [ Add to Search ](https://pubmed.ncbi.nlm.nih.gov/42698010/) * Cell Line, Tumor Actions * [ Search in PubMed ](https://pubmed.ncbi.nlm.nih.gov/?term=%22Cell+Line%2C+Tumor%22%5BMeSH%5D&sort=date&sort_order=desc) * [ Search in MeSH ](https://www.ncbi.nlm.nih.gov/mesh?term=Cell+Line%2C+Tumor) * [ Add to Search ](https://pubmed.ncbi.nlm.nih.gov/42698010/) * Cell Movement Actions * [ Search in PubMed ](https://pubmed.ncbi.nlm.nih.gov/?term=%22Cell+Movement%22%5BMeSH%5D&sort=date&sort_order=desc) * [ Search in MeSH ](https://www.ncbi.nlm.nih.gov/mesh?term=Cell+Movement) * [ Add to Search ](https://pubmed.ncbi.nlm.nih.gov/42698010/) * Cell Proliferation Actions * [ Search in PubMed ](https://pubmed.ncbi.nlm.nih.gov/?term=%22Cell+Proliferation%22%5BMeSH%5D&sort=date&sort_order=desc) * [ Search in MeSH ](https://www.ncbi.nlm.nih.gov/mesh?term=Cell+Proliferation) * [ Add to Search ](https://pubmed.ncbi.nlm.nih.gov/42698010/) * Gene Expression Regulation, Neoplastic Actions * [ Search in PubMed ](https://pubmed.ncbi.nlm.nih.gov/?term=%22Gene+Expression+Regulation%2C+Neoplastic%22%5BMeSH%5D&sort=date&sort_order=desc) * [ Search in MeSH ](https://www.ncbi.nlm.nih.gov/mesh?term=Gene+Expression+Regulation%2C+Neoplastic) * [ Add to Search ](https://pubmed.ncbi.nlm.nih.gov/42698010/) * Humans Actions * [ Search in PubMed ](https://pubmed.ncbi.nlm.nih.gov/?term=%22Humans%22%5BMeSH%5D&sort=date&sort_order=desc) * [ Search in MeSH ](https://www.ncbi.nlm.nih.gov/mesh?term=Humans) * [ Add to Search ](https://pubmed.ncbi.nlm.nih.gov/42698010/) * Liver Neoplasms* / genetics Actions * [ Search in PubMed ](https://pubmed.ncbi.nlm.nih.gov/?term=%22Liver+Neoplasms%2Fgenetics%22%5BMAJR%5D&sort=date&sort_order=desc) * [ Search in MeSH ](https://www.ncbi.nlm.nih.gov/mesh?term=Liver+Neoplasms) * [ Add to Search ](https://pubmed.ncbi.nlm.n
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