Table 3.
Latest applications of scRNA-Seq in cancer research.
| Cancer | Method | Stromal Cell Subtypes | Key Differential Genes | Mechanisms | References |
|---|---|---|---|---|---|
| Gallbladder cancer | 10× Genomics | Lymphocytes | CTLA4 TIGIT |
Immunoproteins CTLA4 and TIGIT are highly expressed in CD8+ T cells, and bile acid and fatty acid metabolism levels are disturbed. | [98] |
| Macrophages | |||||
| Dendritic cells | |||||
| HL | 10× Genomics | Macrophages | LAG3 FOXP3 |
Differential protein LAG3 and FOXP3+ T cells increase, leading to HL. | [99] |
| T cells | |||||
| B cells | |||||
| Lung adenocarcinoma | 10× Genomics | Macrophages | SFTPA2 | High expression of the angiogenic markers VWA1 and HSPG2 through the TGFβ and JAK/STAT signaling pathways lead to an elevated expression of genes, such as EGFR. | [100] |
| NK cells | CXCL9 | ||||
| T cells | EGFR | ||||
| PDAC | 10× Genomics | Endothelial cells Fibroblasts | HIF1A | The expression levels of cell type-specific markers for epithelial–mesenchymal transition (EMT+) cancer cells, activated fibroblasts (CAFs), and endothelial cells are strongly correlated with patient survival. | [101] |
| COL1A1 | |||||
| VEGFA | |||||
| PitNETs | 10× Genomics | Fibro fibroblasts | LHB | The differential gene SOX9 is highly expressed in tumors expressing T-PIT and SF-1 (P11), leading to transcriptional dysregulation in tumors. | [102] |
| Endothelial cells | ZFP36 | ||||
| Immune cells | BTG1 | ||||
| Colorectal cancer | 10× Genomics | Fibroblasts | FABP4 | The Wnt signaling pathway is activated and promotes granulocyte migration, resulting in abnormal ferroptosis. | [103] |
| T cells | SPP1 | ||||
| B Cells | RBP7 | ||||
| Prostate cancer | 10× Genomics | T cells | KRT5 KLK3 TP63 |
Elevated KLK3 in T cells inhibits TNF-α, leading to prostate cancer. | [104] |
| B Cells | |||||
| HGSTOC | 10× Genomics | Lymphatic endothelial cells | COMP | Activation of IL6 and JAK/STAT in fibroblast and HGSTOC cancer cell subsets is involved in pathogenesis. | [105] |
| Myofibroblasts | LTBP2 | ||||
| Plasma cells | TGFBI | ||||
| NSCLC | 10× Genomics | CD8+ T cells | SERPINA9 | Increased expression of CD54 and decreased expression of CD62L in CD8+ T cells led to the development of lung cancer. Furthermore, CD20+ B cells produced low levels of SERPINA9 and directly promoted the growth of non-small lung cancer cells. | [106,107] |
| CD4+ T cells | EGFR | ||||
| B cells | CD83 | ||||
| AITL | 10× Genomics | B Cells | XCL2 | Upregulation of the chemokines XCL2 and XCL1 results in deranged metabolic levels of the biomarkers CD73 and CXCR5 in CD8+ T and AITL CD19+ B cell populations. | [108] |
| T cells | XCL1 | ||||
| Plasma cells | CXCR5 | ||||
| Breast cancer | 10× Genomics | Natural killer cells | BDH2 | Upregulation of aerobic glycolysis and mitochondrial oxidative phosphorylation leads to dysregulation of the metabolic level of CD8+ T cells and T cells. | [109,110,111,112] |
| T cells | DECR1 | ||||
| B cells | PHLDA2 | ||||
| Liver and biliary tumors | 10× Genomics | B cells | MALAT1 | The metabolically dominant organoid HCC272 can remodel the tumor microenvironment by accelerating glucose, enhancing hypoxia-induced HIF-1 signaling, and lead to upregulation of NEAT1 in CD44 cells, thereby inducing hyperactivation of Jak-STAT signaling. | [113] |
| CD44 cells | NEAT1 | ||||
| HCC272 cells | SAT1 |