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Selamectin increases cisplatin sensitivity by inhibiting cisplatin-resistant genes expression and autophagy in uveal melanoma

ABSTRACT: Selamectin increases cisplatin sensitivity by inhibiting cisplatin-resistant genes expression and autophagy in uveal melanoma

PROVIDER: PRJNA949137 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR23977582_1.fastq.gz	Fastqsanger.gz
	SRR23977582_2.fastq.gz	Fastqsanger.gz
	SRR23977583_1.fastq.gz	Fastqsanger.gz
	SRR23977583_2.fastq.gz	Fastqsanger.gz
	SRR23977584_1.fastq.gz	Fastqsanger.gz

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Selamectin increases cisplatin sensitivity by inhibiting cisplatin-resistant genes expression and autophagy in uveal melanoma

Project description:Cisplatin resistance is the main reason for uveal melanoma (UM) treatment failure. Thus, developing strategy that increasing cisplatin sensitivity is needed. In this study, we performed drug repositioning analysis with the Connectivity Map database using a panel of previously identified cisplatin sensitivity–associated genes and cisplatin resistance–associated genes as the signature and obtained the antiparasitic drug selamectin. We demonstrated that the selamectin and cisplatin combination showed a synergistic effect on inhibiting UM cell growth. Experiments in tumor-bearing nude mice further showed that selamectin and cisplatin have synergistic effects in reducing tumor growth. Previous studies have linked increased autophagy with tumor resistance to chemotherapy. We found that selamectin inhibited the expression of the autophagy-related gene ATG9B, thus reducing autophagy. The cisplatin resistance–associated genes PDGFRB, DUSP1, MAST1 and IL11 were significantly downregulated in UM cells treated with selamectin. In summary, our study shows that selamectin enhanced the sensitivity of UM to cisplatin, through the mechanism of inhibiting cisplatin resistance–associated gene expression and autophagy. These findings may provide a new strategy for the treatment of UM.

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BRMS1L promotes chemotherapy sensitivity by inhibiting autophagy in breast cancer

Project description:BRMS1L (Breast cancer metastasis suppressor 1 like), a component of Sin3A-histone deacetylase (HDAC) co-repressor complex, has been shown to provide an epigenetic regulation ofWnt signal pathway and act as a metastasis suppressor in breast cancer. However, the role of BRMS1L in the progression and chemosensitivity has not been explored. In the present study, we for the first time showed that reduced BRMS1L expression correlates with poor response to neoadjuvant chemotherapy and poor prognosis in patients with breast cancer. Additionally, chemoresistant breast cancer cells exhibited decreased BRMS1L expression and increased autophagy levels. Furthermore, ectopic expression of BRMS1L significantly enhanced chemotherapy sensitivity via inhibiting protective autophagy in breast cancer cells. In vivo, the experiments in nude mice showed that BRMS1L strengthened the chemotherapy effects on xenografts. Collectively, these results revealed that BRMS1L enhances chemotherapy sensitivity via inhibiting autophagy. Our findings uncover a novel role of BRMS1L in drug sensitivity and highlight the potential clinical application of BRMS1L in the treatment of breast cancer.

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Project description:Autophagy is important for removal, degradation and recycling of damaged organelles, proteins, and lipids through the degradative action of lysosomes. In addition to its catabolic function, autophagy is important in cancer and viral-mediated tumorigenesis, including Human Papillomavirus (HPV) positive cancers. HPV infection is a major risk factor in a subset of Head and Neck Cancer (HNC), for which no targeted therapies are currently available. Herein, we assessed autophagy function in HPV-positive HNC. We showed that HPV-positive HNC cells presented a transcriptional and functional impairment of autophagic process compared to HPV-negative cells, which was reactivated by knocking-down HPV E6/E7 oncoproteins, the drivers of cellular transformation. We found that the oncoprotein c-MYC was stabilized and triggered in HPV-positive cell lines. This resulted in the reduced binding of the MiT/TFE transcription factors to their autophagy targets due to c-MYC competition. Thus, knock-down of c-MYC induced the upregulation of autophagic and lysosomal genes in HPV-positive HNC cells, as well as the increase of autophagic markers at the protein level. Moreover, HPV oncoprotein E7 upregulated the expression of the phosphatase inhibitor CIP2A, accounting for c-MYC upregulation and stability in HPV+ HNC cells. CIP2A mRNA expression negatively correlated with autophagy gene expression in tumor tissues from HNC patients, showing, for the first time, its implication in a transcriptional autophagic context. Both CIP2A and c-MYC knock-down, as well as pharmacological downregulation of c-MYC, resulted in increased resistance to Cisplatin treatment. Our results not only show a novel way by which HPV oncoproteins manipulate the host machinery, but also provide more insights on the role of autophagy in chemoresistance, with possible implications for targeted HPV-positive HNC therapy.

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Project description:Background: Cisplatin-based chemotherapy is the first-line treatment for patients with advanced bladder cancer (BC). However, the development of cisplatin resistance limits its antitumor effects. While, the mechanism of cisplatin resistance remains unclear. Methods: Bioinformatics techniques were used to analyze genes and pathways associated with cisplatin therapy resistance. A variety of biological techniques were used to identify the role of ITGB4 in cisplatin sensitivity in BC and its potential molecular mechanism. Results: In this study, we demonstrated that ITGB4 plays a key role in regulating the sensitivity of p53 wild-type (WT) BC to cisplatin therapy. Our findings revealed that ITGB4 reduces the sensitivity of BC to cisplatin by inhibiting phosphorylation of the p53-S15 site and promoting MDM2 binding to p53, thereby reducing p53 expression. Additionally, we showed that ITGB4 influences the antitumor effects of MDM2 inhibitors when they are combined with cisplatin therapy. Furthermore, we found that ITGB4 levels were elevated in cisplatin-resistant BC cells, a process mediated by STAT3 activation. The combination of STAT3 inhibitors can enhance the antitumor effect of cisplatin in BC. Conclusions: ITGB4 is a key molecule influencing cisplatin sensitivity in p53 WT BC, and the combination of STAT3 inhibitors can enhance the antitumor effect of cisplatin.

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