ArticleGenes & genomics2026
Inhibition of MID1IP1 induces ferroptosis and suppresses c-Myc expression in colorectal cancer cell.
Article in Genes & genomics, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
0 citing papers in PubMed.
No citing paper in PubMed yet.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors.
Funding
Abstract
backgroundColorectal cancer (CRC) is the third most diagnosed cancer worldwide. Despite treatment advances, CRC still requires novel strategies to overcome drug resistance and metastasis. Midline 1 Interacting Protein 1 (MID1IP1) is highly expressed in cancers and promotes tumor growth through c-Myc-mediated ribosomal protein regulation. We hypothesized that MID1IP1 contributes to CRC progression via c-Myc and ferroptosis.
objectiveTo investigate how MID1IP1 affects metabolic reprogramming, ferroptosis, and migration in CRC.
methodsMID1IP1 was silenced in HCT116 cells using siRNA. Colony formation assays evaluated growth. Western blotting assessed c-Myc, ferroptosis-related proteins, glycolytic enzymes, and EMT markers. Intracellular ROS was measured with a fluorescence probe, and a ferroptosis inhibitor confirmed ferroptotic cell death. Immunofluorescence detected c-Myc and PKM2, while wound healing assays evaluated migration.
resultsMID1IP1 knockdown reduced cell growth and c-Myc stability, lowering glycolysis-related protein expression. GPX4 and other ferroptosis-protective proteins decreased, resulting in ROS accumulation and ferroptosis. Migration was inhibited, with altered EMT marker expression.
conclusionMID1IP1 promotes CRC cell survival by stabilizing c-Myc and preventing ferroptosis, while also influencing migration. These findings suggest that MID1IP1 may serve as a novel biomarker and therapeutic target in CRC.
Indexed as
Identifiers
41343117What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.