ArticlePloS one2014
The anoikis effector Bit1 displays tumor suppressive function in lung cancer cells.
Article in PloS one, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.
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Who cites it
24 citing papers in PubMed, 33 citations in OpenAlex.
- The Duality of Collagens in Metastases of Solid Tumors.International journal of molecular sciences · 2025Review
- Oncolytic Newcastle disease virus promotes tumor cell death via the anoikis effector Bit1 translocation.Virologica Sinica · 2025Article
- BUB1-based risk model predicts prostate cancer prognosis and reveals therapeutic vulnerabilities.European journal of medical research · 2025Article
- Anoikis resistance in gastric cancer: a comprehensive review.Cell death & disease · 2025Review
- Bit1 promotes the progression of gastric cancer by facilitating epithelial-mesenchymal transition and alleviating apoptosis.Medical oncology (Northwood, London, England) · 2025Article
- Metabolic reprogramming and signaling adaptations in anoikis resistance: mechanisms and therapeutic targets.Molecular and cellular biochemistry · 2025Review
- Article
- Ergotamine Targets KIF5A to Facilitate Anoikis in Lung Adenocarcinoma.The clinical respiratory journal · 2024Article
- Deciphering the significance of anoikis in bladder cancer and systematic analysis of S100A7 as a potential therapeutic target.European journal of medical research · 2024Article
- Article
- Clinical value of anoikis-related genes and molecular subtypes identification in bladder urothelial carcinoma andFrontiers in immunology · 2023Article
- Anoikis in phenotypic reprogramming of the prostate tumor microenvironment.Frontiers in endocrinology · 2023Review
- Review
- Roles of transducin-like enhancer of split (TLE) family proteins in tumorigenesis and immune regulation.Frontiers in cell and developmental biology · 2022Review
- Spontaneous Cell Detachment and Reattachment in Cancer Cell Lines: An In Vitro Model of Metastasis and Malignancy.International journal of molecular sciences · 2021Article
- Transducin-Like Enhancer of Split-1 Inhibits Malignant BehaviorsFrontiers in oncology · 2020Article
- Bit1 Silencing Enhances the Proliferation, Migration, and Invasion of Glioma Cells Through Activation of the IL-6/STAT3 Pathway.OncoTargets and therapy · 2020Article
- Identifying gene-gene interactions using penalized tensor regression.Statistics in medicine · 2018Article
- Downregulation of Bit1 expression promotes growth, anoikis resistance, and transformation of immortalized human bronchial epithelial cells via Erk activation-dependent suppression of E-cadherin.Biochemical and biophysical research communications · 2018Article
- TLE1 inhibits anoikis and promotes tumorigenicity in human lung cancer cells through ZEB1-mediated E-cadherin repression.Oncotarget · 2017Article
Corrections and comments
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Authors and funding
9 authors at 2 institutions in 1 country.
Funding
Abstract
The mitochondrial Bit1 (Bcl-2 inhibitor of transcription 1) protein is a part of an apoptotic pathway that is uniquely regulated by integrin-mediated attachment. As an anoikis effector, Bit1 is released into the cytoplasm following loss of cell attachment and induces a caspase-independent form of apoptosis. Considering that anoikis resistance is a critical determinant of transformation, we hypothesized that cancer cells may circumvent the Bit1 apoptotic pathway to attain anchorage-independence and tumorigenic potential. Here, we provide the first evidence of the tumor suppressive effect of Bit1 through a mechanism involving anoikis induction in human lung adenocarcinoma derived A549 cells. Restitution of Bit1 in anoikis resistant A549 cells is sufficient to induce detachment induced-apoptosis despite defect in caspase activation and impairs their anchorage-independent growth. Conversely, stable downregulation of Bit1 in these cells significantly enhances their anoikis resistance and anchorage-independent growth. The Bit1 knockdown cells exhibit significantly enhanced tumorigenecity in vivo. It has been previously shown that the nuclear TLE1 corepressor is a putative oncogene in lung cancer, and we show here that TLE1 blocks Bit1 mediated anoikis in part by sequestering the pro-apoptotic partner of Bit1, the Amino-terminal Enhancer of Split (AES) protein, in the nucleus. Taken together, these findings suggest a tumor suppressive role of the caspase-independent anoikis effector Bit1 in lung cancer. Consistent with its role as a tumor suppressor, we have found that Bit1 is downregulated in human non-small cell lung cancer (NSCLC) tissues.
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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.