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RNA-seq of small cell lung cancer [PolyA RNA-Seq]

ABSTRACT: We used CCK-8 experiment to determine the chemotherapy tolerance of small cell lung cancer cells, from which we found chemotherapy-sensitive cells (H446) and chemotherapy-tolerant cells (SHP77). By RNA-SEQ, we found 972 mRNAs with abnormal expression associated with chemotherapy tolerance, including 560 up-regulated mRNAs and 412 down-regulated mRNAs. Several miRNAs related to chemotherapy tolerance of small cell lung cancer were found through qRT-PCR verification, which helped us to further clarify the mechanism of chemotherapy tolerance of small cell lung cancer.

ORGANISM(S): Homo sapiens

PROVIDER: GSE193852 | GEO | 2023/06/30

REPOSITORIES: GEO

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Project description:MTI-101 is a first-in-class novel cyclic peptide shown to have anti-tumor activity in both multiple myeloma and castrate-resistant prostate in vivo cancer models. These data suggest the potential for a broad spectrum of anti-cancer activity for this class of compounds. To further delineate determinants of sensitivity and resistance that were not dependent on oncogenic drivers, two isogenic drug resistant cell lines were generated with chronic exposure to MTI-101 in a non-small cell lung cancer (NSCLC) PC-9 (EGFR driven) and a small cell lung cancer (SCLC) H446 (PTEN deleted and c-MYC amplified). Using the isogenic cell line systems coupled with RNA-SEQ, the top enriched GSEA hallmark was downregulation of genes that contribute to epithelial to mesenchymal transition (EMT), a finding that was consistent in both acquired MTI-101 selected resistant cell lines. The RNA-SEQ data correlated with predicted changes in the phenotype, including significant decreased invasion in Matrigel and changes of EMT markers (E-Cadherin, Vimentin and Twist) at the protein level. Furthermore, in the EGFR driven PC-9 cell line, selection for resistance towards MTI-101 resulted in collateral sensitivity toward EGFR inhibitors. To determine the stability of the MET phenotype, cells were removed from drug and tested for invasion and drug resistance every month. These data indicated that the mesenchymal to epithelial transition (MET) phenotype and genotype was stable for a minimum of six months. MTI-101 treatment in PC-9 and H446 cells showed synergistic activity with the standard of care agents Erlotinib, Osimertinib, and Cisplatin when used in combination in PC-9 and H446 cells, respectively. Finally, in vivo data indicates that MTI-101 treatment selects for increased E-Cadherin and decreased Vimentin in H446. In addition, treatment with MTI-101 decreased incidence of bone metastasis in the PC-9 in vivo model. Together, these data indicate that MTI-101 treatment could be used as a tool to delay the emergence of metastatic disease for the treatment of lung cancer.

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RNA-seq of small cell lung cancer [PolyA RNA-Seq]

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