Skip to content
DraconiticResearch
Search Sources API
203,203 studies31 sourcesUpdated 42 min ago
Peer-reviewedCC BY 4.0International Journal of Molecular Sciences

MED19 Knockdown Induces G1 Cell-Cycle Arrest Through Downregulation of AREG and CKS1B in Lung and Breast Cancer Cells

  • Sailakshmi Iyer1
  • Naoko Hattori1,2
  • Takeya Nakagawa1
  • Satoshi Fujii3
  • Tomonori Hayashi4
  • Takashi Ito1
4 affiliations
  1. 1Department of Biochemistry, Nagasaki University Graduate School of Biomedical Sciences, Nagasaki 852-8523, Japan
  2. 2Department of Dermatology, Nagasaki University Graduate School of Biomedical Sciences, Nagasaki 852-8523, Japan
  3. 3Department of Bioscience and Bioinformatics, Kyushu Institute of Technology, Fukuoka 804-8550, Japan
  4. 4Radiation Effects Research Foundation, Hiroshima 732-0815, Japan
Open at sourceDOICite

Abstract

Mediator complex subunit 19 (MED19), a component of the Mediator complex, has emerged as a potential regulator of cancer progression, although its downstream transcriptional programs remain poorly understood. Here, we investigated the role of MED19 across 20 human cancer cell lines. An siRNA-mediated knockdown (KD) screen identified A549 lung cancer and MCF-7 breast cancer cells as particularly sensitive to MED19 KD, exhibiting markedly reduced cell viability. Flow cytometric analysis revealed that MED19 KD induced G1-phase arrest, suggesting a role in G1/S-phase progression. RNA sequencing followed by differential expression, Gene Ontology (GO), and chromosomal mapping analyses identified amphiregulin (AREG) and cyclin-dependent kinase regulatory subunit 1B (CKS1B) as candidate downstream effectors in A549 and MCF-7 cells, respectively. Knockdown of AREG or CKS1B inhibited cell proliferation and recapitulated the G1-phase arrest induced by MED19 KD. Moreover, ectopic expression of AREG or CKS1B partially rescued the cell-cycle defects caused by MED19 KD. These findings identify MED19 as a context-dependent regulator of cancer cell proliferation and G1/S-phase progression through distinct downstream transcriptional programs in lung and breast cancer cells.

Related

  1. VIRMA-associated SRD5A2 downregulation promotes BPH progression through ERα-CREB5-dependent epithelial plasticity
    Zhemin Lin, Zhanliang Liu, Mingxin Jiang +7
    iSciencePeer-reviewedCC BY-NC-ND 4.0Molecular biology & gene regulationCell biologyCrossrefCell Press
  2. Downregulation of GJA1-Derived circ_753 and circ_755 Differentially Modulates miR-182-5p Expression and Breast Cancer-Associated Phenotypes
    Nour Maatouk, Joséphine Briand, Jana Ismael +5
    International Journal of Molecular SciencesPeer-reviewedCC BY 4.0Full textMolecular biology & gene regulationCrossrefEurope PMC
  3. Tunlametinib Suppresses Melanogenesis Induces Cell Cycle Arrest and Apoptosis in Giant Congenital Melanocytic Nevus Cells.
    Jin-Ye Guan, Zhuo Chen, Wen-Shang Liu +4
    CancersPeer-reviewedCC BYFull textMolecular biology & gene regulationEurope PMCCrossref
  4. AICAR induces S phase cell cycle arrest in ESCC by targeting the AMPK/mTORC1 and mTORC2/AKT pathway
    Muping Zou, Tianrui Zhang, Lingbin He +12
    Frontiers in OncologyPeer-reviewedCC BY 4.0Full textMolecular biology & gene regulationCrossrefPMC
  5. PTHrP induces breast cancer bone metastases via microbial-dependent expansion of TNF/IL-17–producing T cells
    Nand K. Roy, Subhashis Pal, Hamid Y. Dar +3
    JCI InsightPeer-reviewedCC BY 4.0Full textMolecular biology & gene regulationPMC

Cite

BibTeXRIS
BibTeX
@article{iyer2026med19,
  title = {{MED19 Knockdown Induces G1 Cell-Cycle Arrest Through Downregulation of AREG and CKS1B in Lung and Breast Cancer Cells}},
  author = {Sailakshmi Iyer and Naoko Hattori and Takeya Nakagawa and Satoshi Fujii and Tomonori Hayashi and Takashi Ito},
  journal = {International Journal of Molecular Sciences},
  year = {2026},
  month = nov,
  doi = {10.3390/ijms272110004},
  url = {https://www.mdpi.com/1422-0067/27/21/10004},
  note = {CC BY 4.0},
}
RIS
TY  - JOUR
TI  - MED19 Knockdown Induces G1 Cell-Cycle Arrest Through Downregulation of AREG and CKS1B in Lung and Breast Cancer Cells
AU  - Sailakshmi Iyer
AU  - Naoko Hattori
AU  - Takeya Nakagawa
AU  - Satoshi Fujii
AU  - Tomonori Hayashi
AU  - Takashi Ito
PY  - 2026
DA  - 2026/11/08
JO  - International Journal of Molecular Sciences
DO  - 10.3390/ijms272110004
UR  - https://www.mdpi.com/1422-0067/27/21/10004
AB  - Mediator complex subunit 19 (MED19), a component of the Mediator complex, has emerged as a potential regulator of cancer progression, although its downstream transcriptional programs remain poorly understood. Here, we investigated the role of MED19 across 20 human cancer cell lines. An siRNA-mediated knockdown (KD) screen identified A549 lung cancer and MCF-7 breast cancer cells as particularly sensitive to MED19 KD, exhibiting markedly reduced cell viability. Flow cytometric analysis revealed that MED19 KD induced G1-phase arrest, suggesting a role in G1/S-phase progression. RNA sequencing followed by differential expression, Gene Ontology (GO), and chromosomal mapping analyses identified amphiregulin (AREG) and cyclin-dependent kinase regulatory subunit 1B (CKS1B) as candidate downstream effectors in A549 and MCF-7 cells, respectively. Knockdown of AREG or CKS1B inhibited cell proliferation and recapitulated the G1-phase arrest induced by MED19 KD. Moreover, ectopic expression of AREG or CKS1B partially rescued the cell-cycle defects caused by MED19 KD. These findings identify MED19 as a context-dependent regulator of cancer cell proliferation and G1/S-phase progression through distinct downstream transcriptional programs in lung and breast cancer cells.
SN  - 1422-0067
ER  -