ArticleCancer research2014
CRR9/CLPTM1L regulates cell survival signaling and is required for Ras transformation and lung tumorigenesis.
Article in Cancer research, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 53 papers, 2 of them syntheses that pooled it.
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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.
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Who cites it
53 citing papers in PubMed, 2 syntheses or guidelines pooled it, 71 citations in OpenAlex.
- Genome-wide association study identifies multiple susceptibility loci for pancreatic cancer.Nature genetics · 2014Pooled it
- Cleft lip and palate transmembrane protein 1 rs31489 polymorphism is associated with lung cancer risk: a meta-analysis.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2014Pooled it
- Candidate locus analysis of the TERT-CLPTM1L cancer risk region on chromosome 5p15 identifies multiple independent variants associated with endometrial cancer risk.Human genetics · 2015Trial
- Prioritizing context-specific genetic risk mechanisms in 11 solid cancers.Journal of the National Cancer Institute · 2026Article
- CLPTM1L modulates membrane lipid rafts to promote tumor EGFR signaling.Life metabolism · 2026Article
- Integrative screening identifies functional variants and VNTRs underlying GWAS signals at the 5p15.33 multi-cancer susceptibility locus.medRxiv : the preprint server for health sciences · 2026Article
- Multi-trait and multi-ancestry genetic analysis of comorbid lung diseases and traits improves genetic discovery and polygenic risk prediction.Nature genetics · 2026Article
- Multi-trait analysis of pigmentation traits in relation to skin and ocular cancers: Relevance for evolutionary medicine.Evolution, medicine, and public health · 2026Article
- From locus to gene: causal inference and experimental validation prioritize PSMA4 as a candidate target in lung adenocarcinoma.American journal of cancer research · 2026Article
- ADHD-anchored partitioning of non-small cell lung cancer genetic covariance identifiesFrontiers in immunology · 2026Article
- Prioritizing context-specific genetic risk mechanisms in 11 solid cancers.medRxiv : the preprint server for health sciences · 2025Article
- Isoform-level analyses of 6 cancers uncover extensive genetic risk mechanisms undetected at the gene-level.British journal of cancer · 2025Article
- A genome-wide association study integrated with single-cell and bulk profiles uncovers susceptibility genes for nasopharyngeal carcinoma involved in tumorigenesis via regulation of T cells.Genome biology · 2025Article
- CLPTM1L interacts with ERLIN2 to stabilize SREBP1 and drive tumorigenesis in nasopharyngeal carcinoma.Cell death & disease · 2025Article
- Multi-trait and multi-ancestry genetic analysis of comorbid lung diseases and traits improves genetic discovery and polygenic risk prediction.medRxiv : the preprint server for health sciences · 2024Article
- CLPTM1L is a GPI-anchoring pathway component targeted by HCMV.The Journal of cell biology · 2023Article
- CLPTM1L expression predicts recurrence of patients with intermediate‑ and high‑risk stage IB‑IIB cervical cancer undergoing radical hysterectomy followed by TP as adjuvant chemotherapy.Oncology letters · 2023Article
- Functional characterization of 5p15.33 risk locus in uveal melanoma reveals rs452384 as a functional variant and NKX2.4 as an allele-specific interactor.American journal of human genetics · 2022Article
- Functional studies of lung cancer GWAS beyond association.Human molecular genetics · 2022Review
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Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
The transmembrane protein CLPTM1L is overexpressed in non-small cell lung cancer, where it protects tumor cells from genotoxic apoptosis. Here, we show that RNA interference-mediated blockade of CLPTM1L inhibits K-Ras-induced lung tumorigenesis. CLPTM1L expression was required in vitro for morphologic transformation by H-RasV12 or K-RasV12, anchorage-independent growth, and survival of anoikis of lung tumor cells. Mechanistic investigations indicated that CLPTM1L interacts with phosphoinositide 3-kinase and is essential for Ras-induced AKT phosphorylation. Furthermore that the anti-apoptotic protein Bcl-xL is regulated by CLPTM1L independently of AKT activation. Constitutive activation of AKT or Bcl-xL rescued the transformed phenotype in CLPTM1L-depleted cells. The CLPTM1L gene lies within a cancer susceptibility locus at chromosome 5p15.33 defined by genome-wide association studies. The risk genotype at the CLPTM1L locus was associated with high expression of CLPTM1L in normal lung tissue, suggesting that cis-regulation of CLPTM1L may contribute to lung cancer risk. Taken together, our results establish a protumorigenic role for CLPTM1L that is critical for Ras-driven lung cancers, with potential implications for therapy and chemosensitization.
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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.