ArticleCell communication and signaling : CCS2019
Integral membrane protein 2A inhibits cell growth in human breast cancer via enhancing autophagy induction.
Article in Cell communication and signaling : CCS, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.
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
27 citing papers in PubMed, 50 citations in OpenAlex.
- The emerging roles of ITM2A: At the molecular crossroads of development and pathogenesis.iScience · 2026Review
- The potential ofJournal of thoracic disease · 2025Article
- Machine Learning-Based Gene Expression Analysis to Identify Prognostic Biomarkers in Upper Tract Urothelial Carcinoma.Cancers · 2025Article
- Pooled tagging and hydrophobic targeting of endogenous proteins for unbiased mapping of unfolded protein responses.Molecular cell · 2025Article
- ITM2A as a potential prognostic marker for triple-negative breast cancer.Journal of Cancer · 2025Article
- Multi-omics identification and validation of oxidative phosphorylation-related hub genes in schizophrenia.Frontiers in genetics · 2025Article
- miRNA-1 regulation is necessary for mechanical overload-induced muscle hypertrophy in male mice.Physiological reports · 2025Article
- Article
- Receptor-mediated transcytosis for brain delivery of therapeutics: receptor classes and criteria.Frontiers in drug delivery · 2024Review
- ITM2A inhibits the progression of bladder cancer by downregulating the phosphorylation of STAT3.American journal of cancer research · 2024Article
- HUNK inhibits epithelial-mesenchymal transition of CRC via direct phosphorylation of GEF-H1 and activating RhoA/LIMK-1/CFL-1.Cell death & disease · 2023Article
- Association of ITM2A rs1751094 polymorphism on X chromosome in Korean pediatric patients with autoimmune thyroid disease.Immunity, inflammation and disease · 2023Article
- Differentially Expressed Genes and Molecular Susceptibility to Human Age-Related Diseases.International journal of molecular sciences · 2023Article
- Construction and Validation of a Protein-associated Prognostic Model for Gastrointestinal Cancer.Combinatorial chemistry & high throughput screening · 2023Article
- Review
- TSPAN1 promotes autophagy flux and mediates cooperation between WNT-CTNNB1 signaling and autophagy via theAutophagy · 2021Article
- Review
- Integral Membrane Protein 2A Is a Negative Regulator of Canonical and Non-Canonical Hedgehog Signalling.Cells · 2021Article
- JARID1B promotes colorectal cancer proliferation and Wnt/β-catenin signaling via decreasing CDX2 level.Cell communication and signaling : CCS · 2020Article
- STYK1 promotes autophagy through enhancing the assembly of autophagy-specific class III phosphatidylinositol 3-kinase complex I.Autophagy · 2020Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundBreast cancer is a life-threatening disease in females and the leading cause of mortality among the female population, presenting huge challenges for prognosis and treatment. ITM2A is a member of the BRICHOS superfamily, which are thought to have a chaperone function. ITM2A has been identified to related to ovarian cancer progress recently. However, the biological role of ITM2A in breast cancer remains largely unclear.
methodsQuantitative real-time polymerase chain reaction (qRT-PCR), western blotting assay and immunohistochemistry staining were used to analyzed the expression level of ITM2A. The patient overall survival versus ITM2A expression level was evaluated by Kaplan-Meier analysis. MTT assay, EdU incorporation assay and colony formation assay were used to evaluated the role of ITM2A on breast cancer cell proliferation. Autophagy was explored through autophagic flux detection using a confocal microscope and autophagic vacuoles investigation under a transmission electron microscopy (TEM). In vitro kinase assay was used to investigated the phosphorylation modification of ITM2A by HUNK.
resultsOur data showed that the expression of integral membrane protein 2A (ITM2A) was significantly down-regulated in human breast cancer tissues and cell lines. Kaplan-Meier analysis indicated that patients presenting with reduced ITM2A expression exhibited poor overall survival, and expression significantly correlated with age, progesterone receptor status, TNM classification and tumor stage. ITM2A overexpression significantly inhibited the proliferation of breast cancer cells. By studying several autophagic markers and events in human breast cancer SKBR-3 cells, we further demonstrated that ITM2A is a novel positive regulator of autophagy through an mTOR-dependent manner. Moreover, we found that ITM2A was phosphorylated at T35 by HUNK, a serine/threonine kinase significantly correlated with human breast cancer overall survival and HER2-induced mammary tumorigenesis.
conclusionOur study provided evidence that ITM2A functions as a novel prognostic marker and represents a potential therapeutic target.
Indexed as
Identifiers
What 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.