SP101, a novel synthetic compound reduces the drug resistance of EGFR (T790M) and cancerous stemness in non‐small cell lung carcinoma

Epidermal growth factor receptor (EGFR) mutation at T790M and cancerous stemness have shown the drug resistance of non‐small‐cell lung cancer (NSCLC) in lung cancer therapy. Development of novel drugs in the overcoming drug resistances in the NSCLC therapy is highly desired. SP101 is a novel gefitinib derivative, which can bind the ATP‐binding pocket of EGFR to inhibit its EGFR kinase activity. Interestingly, SP101 has the ability to reduce the drug resistances of EGFR (T790M) and cancerous stemness in NSCLC cells. SP101 displays the anticancer ability in the gefitinib‐resistant EGFR (T790M) of H1975 cells. SP101 inhibited the survivin protein expression and induced the caspase 3 activation and poly ADP‐ribose polymerase (PARP) protein cleavage for apoptosis induction. Moreover, SP101 was effective on the reduction of cell viability in the A549‐ON cells, which expressed Oct4 and Nanog proteins in lung cancer cells displaying cancerous stemness and drug resistance. SP101 inhibited the protein expression of Nanog and Oct4. Taken together, this study demonstrates that SP101 is a novel potential compound in the overcoming drug resistance of NSCLC therapy.

• Publication year

  2016

• Venue

  The FASEB Journal

• Publication date

  2016-04-01

• Fields of study

  Medicine, Chemistry

• Identifiers
  DOI 10.1096/fasebj.30.1_supplement.lb131
• External record

  Open on Semantic Scholar

• Source metadata

  Semantic Scholar

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