ArticleCancer cell international2022
Long non-coding RNA LSAMP-1 is down-regulated in non-small cell lung cancer and predicts a poor prognosis.
Article in Cancer cell international, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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6 citing papers in PubMed, 27 citations in OpenAlex.
- Long Noncoding RNA NKX2-1-AS1 Accelerates Non-Small Cell Lung Cancer Progression through the miR-589-5p/NME1 Axis.Cell biochemistry and biophysics · 2025Article
- Precision Medicine: Transforming Cancer Research through Targeted Therapies.Current genomics · 2025Review
- A novel LINC00478 serves as a tumor suppressor in endometrial carcinoma progression.Journal of cancer research and clinical oncology · 2023Article
- An EMT-related genes signature as a prognostic biomarker for patients with endometrial cancer.BMC cancer · 2023Article
- Article
- Cancer-associated fibroblast-related gene signatures predict survival and drug response in patients with colorectal cancer.Frontiers in genetics · 2022Article
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Authors and funding
14 authors at 6 institutions in 1 country.
Funding
Abstract
backgroundLong noncoding RNAs (lncRNAs) are emerging as master regulators for gene expression and thus play a vital role in human tumorigenesis and progression. But the involvement of novel lncRNAs in non-small cell lung cancer (NSCLC) remains largely unelucidated.
methodsA total of 170 NSCLC and their adjacent non-tumor tissues were enrolled to detect the expression of Lnc-LSAMP-1 by RT-qPCR. The effects of Lnc-LSAMP-1 on cell proliferation, migration, invasion and drug-sensitivity were determined by in vitro and in vivo experiments. The proteins that interact with Lnc-LSAMP-1were confirmed by RNA pull-down assay. RNA-sequencing were used to identify the potential targets of Lnc-LSAMP-1 in NSCLC.
resultsWe found that Lnc-LSAMP-1 was significantly down-regulated in 170 cases of NSCLC tissues when compared to their adjacent non-cancerous tissues. Loss expression of Lnc-LSAMP-1 was notably correlated with unfavorable prognosis of NSCLC patients. The ectopic expression of Lnc-LSAMP-1 drastically inhibited lung cancer cell proliferation, viability, invasion and migration ability, arrested cell cycle and facilitated apoptosis. Chemotherapy sensitization experiments showed that over-expressed Lnc-LSAMP-1 enhanced the inhibition of cell proliferation induced by TKI. Mechanistically, Lnc-LSAMP-1-LSAMP formed a complex which could protect the degradation of LSAMP gene, and thus exerted crucial roles in NSCLC progression and TKI targeted treatment.
conclusionsConsequently, our findings highlight the function and prognostic value of Lnc-LSAMP-1 in NSCLC and provide potential novel therapeutic targets and prognostic biomarkers for patients with NSCLC.
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