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Comprehensive transcriptomic profiles of non-small cell lung cancer by single-cell RNA-seq

ABSTRACT: Comprehensive transcriptomic profiles of non-small cell lung cancer by single-cell RNA-seq

PROVIDER: PRJNA490686 | ENA |

REPOSITORIES: ENA

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Comprehensive transcriptomic profiles of non-small cell lung cancer by single-cell RNA-seq

Project description:Lung cancer has been the leading cause of cancer death seriously threatening human health. The lung cancers display high heterogeneity in terms of pathology and molecular biomarkers. However, previous studies are mainly based on population of cancer cells due to technical limitations, which would conceal important information from rare single cells. Hence, using a modified STRT-seq technique, we profiled transcriptomes of over 9,000 single cells from 20 primary non-small cell lung cancer (NSCLC) patients diagnosed with stage I-IV. We identified major epithelial cell types, stroma cells and immune cells existed in lung, analyzed the differences between normal and tumor tissues and described the heterogeneity of intra- and inter-tumor tissues at single cell level. Furthermore, we analyzed the potential relationship of malignant epithelial cells, stroma cells and immune cells. In summary, our comprehensive analysis provided maps of transcriptomes characteristics of lung cancers and will be helpful for the prognosis and therapy of lung cancers.

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Project description:We have sequenced the genomes of 110 small cell lung cancers (SCLC), one of the deadliest human cancers. We found bi-allelic inactivation of TP53 and RB1 in nearly all the tumors analyzed, sometimes by complex genomic rearrangements. Two tumors with wild-type RB1 had evidence of chromothripsis leading to overexpression of Cyclin D1, revealing an alternative mechanism of Rb1 deregulation. Thus, loss of the tumor suppressors TP53 and RB1 is obligatory in SCLC. We further discovered somatic genomic rearrangements of TP73 that create an oncogenic version of this gene, TP73Δex2/3. In few cases, SCLC tumors exhibited kinase gene mutations, providing a possible therapeutic opportunity for individual patients. Finally, we observed inactivating mutations in NOTCH family genes in 25% of human SCLC. Accordingly, activation of Notch signaling in a pre-clinical SCLC mouse model dramatically reduced the number of tumors and extended the survival of the mutant mice. Furthermore, neuroendocrine gene expression was abrogated by Notch activity in SCLC cells. This first comprehensive study of somatic genome alterations in SCLC uncovers several key biological processes and identifies candidate therapeutic targets in this highly lethal form of cancer.

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Project description:We have sequenced the genomes of 110 small cell lung cancers (SCLC), one of the deadliest human cancers. In nearly all the tumours analysed we found bi-allelic inactivation of TP53 and RB1, sometimes by complex genomic rearrangements. Two tumours with wild-type RB1 had evidence of chromothripsis leading to overexpression of cyclin D1 (encoded by the CCND1 gene), revealing an alternative mechanism of Rb1 deregulation. Thus, loss of the tumour suppressors TP53 and RB1 is obligatory in SCLC. We discovered somatic genomic rearrangements of TP73 that create an oncogenic version of this gene, TP73?ex2/3. In rare cases, SCLC tumours exhibited kinase gene mutations, providing a possible therapeutic opportunity for individual patients. Finally, we observed inactivating mutations in NOTCH family genes in 25% of human SCLC. Accordingly, activation of Notch signalling in a pre-clinical SCLC mouse model strikingly reduced the number of tumours and extended the survival of the mutant mice. Furthermore, neuroendocrine gene expression was abrogated by Notch activity in SCLC cells. This first comprehensive study of somatic genome alterations in SCLC uncovers several key biological processes and identifies candidate therapeutic targets in this highly lethal form of cancer.

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