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Effect of lysosomal alkalinization on nutrient-rich and nutrient-depleted Caco-2 cells

ABSTRACT: Effect of lysosomal alkalinization on nutrient-rich and nutrient-depleted Caco-2 cells

PROVIDER: PRJNA1028281 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR26387859_1.fastq.gz	Fastqsanger.gz
	SRR26387859_2.fastq.gz	Fastqsanger.gz
	SRR26387860_1.fastq.gz	Fastqsanger.gz
	SRR26387860_2.fastq.gz	Fastqsanger.gz
	SRR26387861_1.fastq.gz	Fastqsanger.gz

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Effect of lysosomal alkalinization on nutrient-rich and nutrient-depleted Caco-2 cells

Project description:Nutrient restriction in cancer cells can activate a number of stress response pathways for cell survival. We aimed to determine mechanistically how nutrient depletion (ND) in colorectal cancer (CRC) cells leads to cellular adaptation. Caco-2 cells under ND showed high viability, tumor-forming ability, and increased expression of one or more epithelial and mesenchymal markers, suggesting the activation of partial (p)-EMT. Lysosomes are activated with ND; therefore, we incubated the ND cells with the V-ATPase inhibitor Bafilomycin A1 (ND+Baf). We observed a further increase in p-EMT markers, numerous membrane protrusions, decreased cell-cell adhesion in 3D, and increased motility in ND+Baf Caco-2 cells. The protrusions in the ND+Baf cells were primarily mediated by microtubules and enabled the relocalization of lysosomes from the perinuclear region to the periphery. Overall, our data show that ND activated p-EMT in CRC cells, which was exacerbated with lysosomal alkalinization.

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Project description:Differentiation is critical for epithelial cell fate decisions, but the signals involved remain unclear. The kidney proximal tubule (PT) cells reabsorb disulphide-rich proteins through endocytosis, generating cystine via lysosomal proteolysis. Here we report that defective cystine mobilization from lysosomes through cystinosin (CTNS), which is mutated in cystinosis, diverts PT cells towards growth and proliferation, disrupting their functions. Mechanistically, lysosomal cystine storage stimulates Ragulator-Rag GTPase-dependent recruitment of mechanistic target of Rapamycin complex 1 (mTORC1) and its constitutive activation. Re-introduction of CTNS restores nutrient-dependent regulation of mTORC1 in knockout cells, whereas cell-permeant analogues of L-cystine, accumulating within lysosomes, render wild-type cells resistant to nutrient withdrawal. Therapeutic mTORC1 inhibition corrects lysosome and differentiation downstream of cystine storage, and phenotypes in a zebrafish model of cystinosis. Thus, cystine serves as a lysosomal signal that tailors mTORC1 signaling and metabolism to direct epithelial cell fate decisions. These results identify mechanisms and therapeutic targets for dysregulated homeostasis in cystinosis.

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