ArticleTranslational cancer research2020
Inhibition of osteopontin overcomes acquired resistance to afatinib in EGFR-mutant non-small-cell lung cancer.
Article in Translational cancer research, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
1 citing paper in PubMed, 2 citations in OpenAlex.
- Osteopontin and Cancer: Insights into Its Role in Drug Resistance.Biomedicines · 2023Review
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 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundWe aimed to explore a novel therapeutic strategy to conquer acquired resistance to second generation EGFR-TKI afatinib in EGFR-mutant NSCLC.
methodsFirstly, we established afatinib-resistant cell lines using increasing concentrations of afatinib. Secondly, we over-expressed or silenced the expression of osteopontin (OPN) using in-vitro transfection. Further, western blot analysis was used to detect the expressions of OPN and epithelial-mesenchymal transition (EMT) biomarkers. Finally, cell proliferation was evaluated by MTT assay.
resultsAfatinib (≤5.0 µmol/L)-resistant H1650 (H1650-AR) and H1975 (H1975-AR) cells were successfully established, and grew faster compared with both parental cells at the same time interval. Western blot analysis revealed that afatinib significantly promoted the expressions of OPN and EMT biomarkers in H1975-AR and H1650-AR cells. Gain and loss assays validated that OPN over-expression promoted acquired resistance to afatinib, and induced the expressions of EMT biomarkers in H1650-AR and H1975-AR cells. Conversely, silencing of OPN not only significantly sensitized resistant cells to afatinib, but also suppressed EMT progression in H1650-AR and H1975-AR cells.
conclusionsThese results demonstrated that OPN was required for acquired resistance of EGFR-mutant NSCLC cells to afatinib.
Indexed as
Identifiers
What Socratic holds
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 Socratic graph.