ArticleMedical oncology (Northwood, London, England)2014
LMO1 is a novel oncogene in lung cancer, and its overexpression is a new predictive marker for anti-EGFR therapy.
Article in Medical oncology (Northwood, London, England), 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers, 1 of them a synthesis that pooled it.
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Who cites it
10 citing papers in PubMed, 1 synthesis or guideline pooled it, 14 citations in OpenAlex.
- LMO1 polymorphisms and the risk of neuroblastoma: Assessment of meta-analysis of case-control studies.Journal of cellular and molecular medicine · 2020Pooled it
- Utilizing single-cell data for per-cell type eQTL mapping in the human pancreas.bioRxiv : the preprint server for biology · 2026Article
- LMO family gene polymorphisms and Wilms tumor susceptibility in Chinese children: a five-center case-control study.BMC cancer · 2024Article
- Comprehensive Analyses and Immunophenotyping of LIM Domain Family Genes in Patients with Non-Small-Cell Lung Cancer.International journal of molecular sciences · 2023Article
- Effect of T-cadherin on the AKT/mTOR signaling pathway, gastric cancer cell cycle, migration and invasion, and its association with patient survival rate.Experimental and therapeutic medicine · 2019Article
- Article
- LMO1 functions as an oncogene by regulating TTK expression and correlates with neuroendocrine differentiation of lung cancer.Oncotarget · 2018Article
- Clinical significance of LMO1 in gastric cancer tissue and its association with apoptosis of cancer cells.Oncology letters · 2017Article
- Hmga2 collaborates withBlood advances · 2017Article
- LMO1 gene polymorphisms contribute to decreased neuroblastoma susceptibility in a Southern Chinese population.Oncotarget · 2016Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Non-small cell lung cancer (NSCLC) is the leading cause of cancer mortality in the world. We report that one oncogene amplified on chromosome 3q26, LMO1, a master transcriptional regulator of stemness, operates to drive strong growth phenotype in NSCLC. We first validate gene expression changes of LMO genes by real-time quantitative RT-PCR real-time quantitative reverse transcriptase-polymerase chain reaction analysis and immunohistochemistry, and we identified gene overexpression of LMO1 compared with non-cancerous tissues (p < 0.01). Next, we discovered that LMO1 promoted cancer cell proliferation in our in vitro/vivo cell proliferation assay, and our cell signaling experiments showed that LMO1 expression correlated with elevated AKT phosphorylation in NSCLC, while the AKT phosphorylation was required for LMO1's oncogenic effects. In addition, we compared complete response rate, stable disease rate, disease progression rate, and the disease control rate of patient with different LMO1 gene expression which pointed to the usefulness of LMO1 overexpression, as a new predictive marker for responsiveness to cetuximab. All in all, LMO1 is a commonly activated tumor promoter that activates AKT signaling in NSCLC and a new predictive marker for targeted therapy.
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