Dataset Information

Targeting claudin-3 suppresses stem cell-like phenotype in nonsquamous non-small-cell lung carcinoma.

ABSTRACT:

Aim

To determine the role of claudin-3 in cancer stemness in nonsquamous non-small-cell lung carcinoma (NSCLC).

Materials & methods

In vitro/vivo extreme limiting dilution analysis and the side population assay were used to investigate the role of claudin-3 in regulating cancer stemness in nonsquamous NSCLC.

Results & conclusion

Claudin-3 depletion decreased the formation rates of spheres and tumors and increased cisplatin sensitivity. Claudin-3 was also identified as one downstream target of estrogen receptor-α in regulating cancer stemness. Moreover, targeting CLDN-3 transcription by small molecules including withaferin A, estradiol and fulvestrant suppressed cancer stemness and reversed chemoresistance. These results demonstrated claudin-3 is one positive regulator of cancer stemness in nonsuqamous NSCLC.

SUBMITTER: Ma L

PROVIDER: S-EPMC6488947 | biostudies-literature | 2019 Feb

REPOSITORIES: biostudies-literature

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Publications

Targeting claudin-3 suppresses stem cell-like phenotype in nonsquamous non-small-cell lung carcinoma.

Ma Lin L Yin Wu W Ma Heliang H Elshoura Ihab I Wang Lan L

Lung cancer management 20190226 1

<h4>Aim</h4>To determine the role of claudin-3 in cancer stemness in nonsquamous non-small-cell lung carcinoma (NSCLC).<h4>Materials & methods</h4><i>In vitro/vivo</i> extreme limiting dilution analysis and the side population assay were used to investigate the role of claudin-3 in regulating cancer stemness in nonsquamous NSCLC.<h4>Results & conclusion</h4>Claudin-3 depletion decreased the formation rates of spheres and tumors and increased cisplatin sensitivity. Claudin-3 was also identified a ...[more]

PMID: 31044015

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Project description:BackgroundNivolumab, a fully human IgG4 programmed death 1 (PD-1) immune-checkpoint-inhibitor antibody, disrupts PD-1-mediated signaling and may restore antitumor immunity.MethodsIn this randomized, open-label, international phase 3 study, we assigned patients with nonsquamous non-small-cell lung cancer (NSCLC) that had progressed during or after platinum-based doublet chemotherapy to receive nivolumab at a dose of 3 mg per kilogram of body weight every 2 weeks or docetaxel at a dose of 75 mg per square meter of body-surface area every 3 weeks. The primary end point was overall survival.ResultsOverall survival was longer with nivolumab than with docetaxel. The median overall survival was 12.2 months (95% confidence interval [CI], 9.7 to 15.0) among 292 patients in the nivolumab group and 9.4 months (95% CI, 8.1 to 10.7) among 290 patients in the docetaxel group (hazard ratio for death, 0.73; 96% CI, 0.59 to 0.89; P=0.002). At 1 year, the overall survival rate was 51% (95% CI, 45 to 56) with nivolumab versus 39% (95% CI, 33 to 45) with docetaxel. With additional follow-up, the overall survival rate at 18 months was 39% (95% CI, 34 to 45) with nivolumab versus 23% (95% CI, 19 to 28) with docetaxel. The response rate was 19% with nivolumab versus 12% with docetaxel (P=0.02). Although progression-free survival did not favor nivolumab over docetaxel (median, 2.3 months and 4.2 months, respectively), the rate of progression-free survival at 1 year was higher with nivolumab than with docetaxel (19% and 8%, respectively). Nivolumab was associated with even greater efficacy than docetaxel across all end points in subgroups defined according to prespecified levels of tumor-membrane expression (≥1%, ≥5%, and ≥10%) of the PD-1 ligand. Treatment-related adverse events of grade 3 or 4 were reported in 10% of the patients in the nivolumab group, as compared with 54% of those in the docetaxel group.ConclusionsAmong patients with advanced nonsquamous NSCLC that had progressed during or after platinum-based chemotherapy, overall survival was longer with nivolumab than with docetaxel. (Funded by Bristol-Myers Squibb; CheckMate 057 ClinicalTrials.gov number, NCT01673867.).

Dataset Information

Targeting claudin-3 suppresses stem cell-like phenotype in nonsquamous non-small-cell lung carcinoma.

Aim

Materials & methods

Results & conclusion

Publications

Targeting claudin-3 suppresses stem cell-like phenotype in nonsquamous non-small-cell lung carcinoma.

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