ArticleCells2020
Colocalization of MID1IP1 and c-Myc is Critically Involved in Liver Cancer Growth via Regulation of Ribosomal Protein L5 and L11 and CNOT2.
Article in Cells, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.
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Who cites it
26 citing papers in PubMed, 42 citations in OpenAlex.
- CNOT2 /c-Myc/STAT3 signaling is critically involved in glycolysis mediated apoptosis of benzyl isothiocyanate in hepatocellular carcinoma.Scientific reports · 2026Article
- Elucidating the Role ofCurrent issues in molecular biology · 2025Review
- Ribosomal protein L5 induces cellular senescence via p53-p21-pRb pathway to mediate relapse of acute myeloid leukemia.Scientific reports · 2025Article
- SNORA47 affects stemness and chemotherapy sensitivity via EBF3/RPL11/c-Myc axis in luminal A breast cancer.Molecular medicine (Cambridge, Mass.) · 2025Article
- RNA-Binding Motif Protein 22 Induces Apoptosis via c-Myc Pathway in Colon Cancer Cells.Molecules (Basel, Switzerland) · 2025Article
- Long-lasting sex-specific alteration in left ventricular cardiac transcriptome following gamma and simGCRsim radiation.Scientific reports · 2025Article
- Ribosomal proteins in hepatocellular carcinoma: mysterious but promising.Cell & bioscience · 2024Review
- Article
- Acetylcorynoline Induces Apoptosis and G2/M Phase Arrest through the c-Myc Signaling Pathway in Colon Cancer Cells.International journal of molecular sciences · 2023Article
- Identification and validation of functional roles for three MYC-associated genes in hepatocellular carcinoma.Journal of advanced research · 2023Article
- Momordicae Semen inhibits migration and induces apoptotic cell death by regulating c-Myc and CNOT2 in human pancreatic cancer cells.Scientific reports · 2023Article
- The Potential Role of Timosaponin-AIII in Cancer Prevention and Treatment.Molecules (Basel, Switzerland) · 2023Review
- Article
- RPL11 promotes non-small cell lung cancer cell proliferation by regulating endoplasmic reticulum stress and cell autophagy.BMC molecular and cell biology · 2023Article
- Ribosome biogenesis in disease: new players and therapeutic targets.Signal transduction and targeted therapy · 2023Review
- Hippo signaling and histone methylation control cardiomyocyte cell cycle re-entry through distinct transcriptional pathways.PloS one · 2023Article
- Ribosomal protein RPL5 regulates colon cancer cell proliferation and migration through MAPK/ERK signaling pathway.BMC molecular and cell biology · 2022Article
- The Antitumor Effect of Timosaponin A3 through c-Myc Inhibition in Colorectal Cancer Cells and Combined Treatment Effect with 5-FU or Doxorubicin.International journal of molecular sciences · 2022Article
- Regulation of Lipid Metabolism by Lamin in Mutation-Related Diseases.Frontiers in pharmacology · 2022Review
- Ophiopogonin D increase apoptosis by activating p53Frontiers in pharmacology · 2022Article
Corrections and comments
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Authors and funding
8 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Though midline1 interacting protein 1 (MID1IP1) was known as one of the glucose-responsive genes regulated by carbohydrate response element binding protein (ChREBP), the underlying mechanisms for its oncogenic role were never explored. Thus, in the present study, the underlying molecular mechanism of MID1P1 was elucidated mainly in HepG2 and Huh7 hepatocellular carcinoma cells (HCCs). MID1IP1 was highly expressed in HepG2, Huh7, SK-Hep1, PLC/PRF5, and immortalized hepatocyte LX-2 cells more than in normal hepatocyte AML-12 cells. MID1IP1 depletion reduced the viability and the number of colonies and also increased sub G1 population and the number of TUNEL-positive cells in HepG2 and Huh7 cells. Consistently, MID1IP1 depletion attenuated pro-poly (ADP-ribose) polymerase (pro-PARP), c-Myc and activated p21, while MID1IP1 overexpression activated c-Myc and reduced p21. Furthermore, MID1IP1 depletion synergistically attenuated c-Myc stability in HepG2 and Huh7 cells. Of note, MID1IP1 depletion upregulated the expression of ribosomal protein L5 or L11, while loss of L5 or L11 rescued c-Myc in MID1IP1 depleted HepG2 and Huh7 cells. Interestingly, tissue array showed that the overexpression of MID1IP1 was colocalized with c-Myc in human HCC tissues, which was verified in HepG2 and Huh7 cells by Immunofluorescence. Notably, depletion of CCR4-NOT2 (CNOT2) with adipogenic activity enhanced the antitumor effect of MID1IP1 depletion to reduce c-Myc, procaspase 3 and pro-PARP in HepG2, Huh7 and HCT116 cells. Overall, these findings provide novel insight that MID1IP1 promotes the growth of liver cancer via colocalization with c-Myc mediated by ribosomal proteins L5 and L11 and CNOT2 as a potent oncogenic molecule.
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