ArticleCell death & disease2020
Kinesin light chain 4 as a new target for lung cancer chemoresistance via targeted inhibition of checkpoint kinases in the DNA repair network.
Article in Cell death & disease, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
What it found
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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.
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Who cites it
9 citing papers in PubMed, 15 citations in OpenAlex.
- Silencing of Kinesin Light Chain 1 Suppresses Aggressive Phenotypes in Cholangiocarcinoma Cells Through Transcriptomic Alterations.International journal of molecular sciences · 2026Article
- KLC3 drives gastric cancer progression by stabilizing SLC2A5 to activate MAPK signaling and promote epithelial-mesenchymal transition.BMC cancer · 2025Article
- Kinesin superfamily proteins in ovarian cancer: from molecular mechanisms to clinical applications.Medical oncology (Northwood, London, England) · 2025Review
- KLC3 activates PI3K/AKT signaling and promotes ovarian cancer cell proliferation and migration through COL3A1.Oncology reports · 2025Article
- scStateDynamics: deciphering the drug-responsive tumor cell state dynamics by modeling single-cell level expression changes.Genome biology · 2024Article
- A humanized Caenorhabditis elegans model of hereditary spastic paraplegia-associated variants in KLC4.Disease models & mechanisms · 2023Article
- A humanizedbioRxiv : the preprint server for biology · 2023Article
- [Cell Cycle Checkpoint Kinase and Drug Resistance of Lung Cancer].Zhongguo fei ai za zhi = Chinese journal of lung cancer · 2021Review
- Heritable Tissue-Specific Gene Expression Associates With Chronic Wound Microbial Species.Wound repair and regeneration : official publication of the Wound Healing Society [and] the European Tissue Repair SocietyArticle
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
13 authors at 5 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The poor therapeutic efficacy of non-small cell lung cancer (NSCLC) is partly attributed to the acquisition of chemoresistance. To investigate the mechanism underlying this resistance, we examined the potential link between kinesin light chain 4 (KLC4), which we have previously reported to be associated with radioresistance in NSCLC, and sensitivity to chemotherapy in human lung cancer cell lines. KLC4 protein levels in lung cancer cells correlated with the degree of chemoresistance to cisplatin treatment. Furthermore, KLC4 silencing enhanced the cytotoxic effect of cisplatin by promoting DNA double-strand breaks and apoptosis. These effects were mediated by interaction with the checkpoint kinase CHK2, as KLC4 knockdown increased CHK2 activation, which was further enhanced in combination with cisplatin treatment. In addition, KLC4 and CHEK2 expression levels showed negative correlation in lung tumor samples from patients, and KLC4 overexpression correlated negatively with survival. Our results indicate a novel link between the KLC4 and CHK2 pathways regulating DNA damage response in chemoresistance, and highlight KLC4 as a candidate for developing lung cancer-specific drugs and customized targeted molecular therapy.
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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.