Modulatory Effect of Prodigiosin or Pioglitazone on TIME and the Crosstalk to Immune-Checkpoint Protein(s)

Condition(s) studied

Study summary

Lung cancer is one of the most common and serious types of cancer. Lung tumor cells exploit immune checkpoint proteins (ICPs) to maintain immune tolerance and thus promote tumor progression and invasion. Inhibition of ICPs using antibody therapies is one of the most common approaches for the treatment of lung cancer. Unfortunately, these antibody-based therapies can lead to severe adverse events. Moreover, a significant number of patients do not respond to immune checkpoint inhibition due to tumor heterogeneity and the immunosuppressive tumor immune microenvironment (TIME). The use of small molecule targeted approach instead of antagonizing antibodies may have the potential advantage of being able to target multiple ICPs in TIME with a single agent as well as improved tumor distribution.

Eligibility

Primary outcome measure(s)

• Gene Expression (mRNA levels) — 36 months
  mRNA levels of HSP90, IL-6, STAT3,c-MYC and the novel immune checkpoint proteins by qRT-PCR from blood samples collected from NSCLC patients and cell pellets collected from lung cancer cell lines before and after pioglitazone or prodigiosin treatment
• Gene Expression (Protein levels) — 36 months
  Protein levels of HSP90, IL-6, STAT3,c-MYC and the novel immune checkpoint proteins by immunoblotting from blood samples collected from NSCLC patients and cell pellets collected from lung cancer cell lines before and after pioglitazone or prodigiosin treatment
• cytotoxic effect — 36 months
  Cytotoxic effect of prodigiosin or pioglitazone on lung cancer cell line using MTT assay
• Anti-cancer efficiency of drug-loaded nanoparticles — 36 months
  Anticancer efficiency against lung cancer in vivo model using Urethan as lung cancer inducer or in vitro lung cancer cell line

Trial sites (1)

More Ain Shams University trials in Egypt

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