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Colorectal cancer cells possess an equipotent capacity to enter a reversible diapause-like state to survive chemotherapy

ABSTRACT: Colorectal cancer cells possess an equipotent capacity to enter a reversible diapause-like state to survive chemotherapy

PROVIDER: PRJNA606811 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR11091545_1.fastq.gz	Fastqsanger.gz
	SRR11091545_2.fastq.gz	Fastqsanger.gz
	SRR11091546_1.fastq.gz	Fastqsanger.gz
	SRR11091546_2.fastq.gz	Fastqsanger.gz
	SRR11091547_1.fastq.gz	Fastqsanger.gz

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Colorectal cancer cells possess an equipotent capacity to enter a reversible diapause-like state to survive chemotherapy

Project description:Cancer cells enter a reversible drug tolerant persister (DTP) state to evade death from chemotherapies and targeted agents. It is increasingly appreciated that DTPs are an important driver of therapy failure and tumor relapse. We combined cellular barcoding and mathematical modeling in patient-derived colorectal cancer models to identify and characterize DTPs in response to chemotherapy. Barcode analysis revealed no loss in clonal complexity of tumors that entered the DTP state and recurred following treatment cessation. Our data fits a mathematical model where all cancer cells, and not a small subpopulation, possess an equipotent capacity to become DTPs. Mechanistically, we determined that DTPs display remarkable transcriptional and functional similarities to diapause, a reversible state of suspended embryonic development triggered by unfavorable environmental conditions. Our study provides insight into how cancer cells use a developmentally conserved mechanism to drive the DTP state pointing to novel therapeutic opportunities to target DTPs.

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Colorectal cancer cells possess an equipotent capacity to enter a developmental pausing-like state to survive chemotherapy

Project description:Cancer cells enter a reversible drug tolerant persister (DTP) state to evade death from both chemotherapies and targeted agents. It is increasingly appreciated that the DTP state is an important driver of therapy failure and tumor relapse. We combined cellular barcoding and mathematical modeling in patient-derived colorectal cancer xenograft models to identify and characterize the cancer cells capable of generating DTPs in response to standard-of-care chemotherapy. Barcode analysis revealed no loss in clonal complexity of tumors that entered the DTP state and recurred following treatment cessation. Our data fits a mathematical model in which all cancer cells, and not a small subpopulation, possess an equipotent capacity to enter the DTP state. Mechanistically, we determined that DTPs display remarkable transcriptional and functional similarities to diapause, a reversible state of suspended embryonic development triggered by unfavorable environmental conditions. Our study provides new insights into how cancer cells use a developmentally conserved mechanism to drive the DTP state pointing to novel therapeutic opportunities to target diapause-like DTPs.

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Global transcriptome analysis of orange wheat blossom midge, Sitodiplosis mosellana (Gehin) (Diptera: Cecidomyiidae) to identify candidate transcripts regulating diapause

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Project description:Cancer cells enter an adaptive persistence to survive radiotherapy and repopulate tumor 1

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Global transcriptome analysis of orange wheat blossom midge, Sitodiplosis mosellana (Gehin) (Diptera: Cecidomyiidae) to identify candidate transcripts regulating diapause

Project description:Many insects enter a developmental arrest (diapause) that allows them to survive harsh seasonal conditions. Despite the well-established ecological significance of diapause, the molecular basis of this crucial adaptation remains largely unresolved. Sitodiplosis mosellana (Gehin), the orange wheat blossom midge (OWBM), causes serious damage to wheat throughout the northern hemisphere, and sporadic outbreaks occur in the world. Traits related to diapause appear to be important factors contributing to their rapid spread and outbreak. To better understand the diapause mechanisms of OWBM, we sequenced the transcriptome and determined the gene expression profile of this species. Examination of different gene expression in DOL and NDOL Total RNA was extracted separately from DOL and NDOL using Trizol Reagent following manufacturer’s instructions. Approximately 10μg RNA from each sample was used to construct individual DGE libraries. mRNA was isolated as described under cDNA library construction. The cDNA fragments were purified by agarose gel electrophoresis and enriched by PCR amplification. Each library had an insert size of 200 bp, and 42 - 50 bp sequences were generated by Illumina HiSeq 2000 in a single run using paired-end technology. SRA Study SRP019201.

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Project description:Cancer cells enter a reversible drug-tolerant persister (DTP) state to evade death from chemotherapy and targeted agents. It is increasingly appreciated that DTPs are important drivers of therapy failure and tumor relapse. We combined cellular barcoding and mathematical modeling in patient-derived colorectal cancer models to identify and characterize DTPs in response to chemotherapy. Barcode analysis revealed no loss of clonal complexity of tumors that entered the DTP state and recurred following treatment cessation. Our data fit a mathematical model where all cancer cells, and not a small subpopulation, possess an equipotent capacity to become DTPs. Mechanistically, we determined that DTPs display remarkable transcriptional and functional similarities to diapause, a reversible state of suspended embryonic development triggered by unfavorable environmental conditions. Our study provides insight into how cancer cells use a developmentally conserved mechanism to drive the DTP state, pointing to novel therapeutic opportunities to target DTPs.

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Project description:Tumor cell repopulation represents a critical factor in the failure of radiotherapy. Analogous to the concept of “drug-tolerant persistence (DTP)” in stress of chemo- or targeted therapy, here, we show that cancer cells enter a “radiation-tolerant persistence (RTP)” to survive radiotherapy and repopulate tumor. These RTP cells exhibit a distinct phenotype characterized by enlargement of cell sizes and nucleus, complex karyotype, cell cycle arrest and engagement of quiescence. A fraction of RTPs unexpectedly give birth to mitotic-competent progeny cells via a viral budding-mimicking cell division. To gain insight into the molecular mechanisms how RTPs generating progenies and repopulating tumors, we applied single cell SMART RNA-sequencing and 10x RNA-sequencing to different status of human colorectal cancer cells HCT116 before and exposed to irradiation. For the first time, we profiled two transitional transcriptional waves throughout budding process and characterized two gene panels associated with budding of RTPs, illustrating the therapeutic potential for blocking tumor repopulation after radiation.

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