Ask about this productRelated genes to: SCAND1 antibody
- Gene:
- SCAND1 NIH gene
- Name:
- SCAN domain containing 1
- Previous symbol:
- -
- Synonyms:
- SDP1, RAZ1
- Chromosome:
- 20q11.23
- Locus Type:
- gene with protein product
- Date approved:
- 2000-06-16
- Date modifiied:
- 2016-10-05
Related products to: SCAND1 antibody
Related articles to: SCAND1 antibody
- Epithelial compartments play a central role in the progression and metastasis of colorectal cancer (CRC), yet the mechanisms underlying their transcriptional reprogramming across disease stages remain incompletely understood. - Source: PubMed
Publication date: 2025/11/24
Xu ChengyuanPan YunZhang SiqiLin MoubinLiu HailongYu Zicheng - In this research, we conducted an in-depth analysis of differentially expressed genes associated with mitochondrial depolarisation in non-small cell lung cancer (NSCLC) using single-cell sequencing. By combining our findings with cuproptosis-related genes, we identified 10 significant risk genes: DCN, PTHLH, CRYAB, HMGCS1, DSG3, ZFP36L2, SCAND1, NUDT4, NDUFA4L2 and RPL36A, using univariate Cox regression analysis and machine learning methods. These genes form the core of our prognosis risk prediction model, which demonstrated high specificity and accuracy in predicting patient outcomes, as evidenced by ROC curve analysis. Kaplan-Meier curves further confirmed that patients in the low-risk group had significantly better survival rates compared to those in the high-risk group. Our models also provided valuable insights into the tumour microenvironment, immunotherapy sensitivity and chemotherapy response. To facilitate the quantification of the probability of patient survival, we incorporated clinical data into a nomogram. We comprehensively analysed the mutation status and expression patterns of the 10 risk genes using bulk transcriptomic, single-cell and spatial transcriptomic datasets. Drug target predictions highlighted DSG3, PTHLH, ZFP36L2, DCN and NDUFA4L2 as promising therapeutic targets. Notably, RPL36A emerged as a potential tumour marker for NSCLC, with its expression validated in lung cancer cell lines through qPCR. This study has established a predictive models based on mitochondrial depolarisation genes associated with cuproptosis, aiding clinicians in forecasting overall survival and guiding personalised treatment strategies. The identification of novel tumour markers has paved the way for targeted therapies, and therapeutic targets are critical for advancing the treatment of NSCLC. - Source: PubMed
Lyu GuoqingDai LihuaDeng XinLiu XiankaiGuo YanZhang YuanWang XiufengHuang YanWu SunGuo Jin-ChengLiu Yanting - Breast cancer (BC) poses a serious threat to human health. Disulfidptosis is a recently discovered form of cell death associated with cancer prognosis and progression. However, the relationship between BC and disulfidptosis remains unclear. - Source: PubMed
Publication date: 2023/12/05
Chen XiongHu GuohuangYu Qianle - The cell stress response is an essential system present in every cell for responding and adapting to environmental stimulations. A major program for stress response is the heat shock factor (HSF)-heat shock protein (HSP) system that maintains proteostasis in cells and promotes cancer progression. However, less is known about how the cell stress response is regulated by alternative transcription factors. Here, we show that the SCAN domain (SCAND)-containing transcription factors (SCAN-TFs) are involved in repressing the stress response in cancer. SCAND1 and SCAND2 are SCAND-only proteins that can hetero-oligomerize with SCAN-zinc finger transcription factors, such as MZF1(ZSCAN6), for accessing DNA and transcriptionally co-repressing target genes. We found that heat stress induced the expression of SCAND1, SCAND2, and MZF1 bound to gene promoter regions in prostate cancer cells. Moreover, heat stress switched the transcript variants' expression from long noncoding RNA (lncRNA-SCAND2P) to protein-coding mRNA of SCAND2, potentially by regulating alternative splicing. High expression of correlated with poorer prognoses in several cancer types, although SCAND1 and MZF1 blocked the heat shock responsiveness of in prostate cancer cells. Consistent with this, gene expression of , , and was negatively correlated with gene expression in prostate adenocarcinoma. By searching databases of patient-derived tumor samples, we found that MZF1 and SCAND2 RNA were more highly expressed in normal tissues than in tumor tissues in several cancer types. Of note, high RNA expression of SCAND2, SCAND1, and MZF1 correlated with enhanced prognoses of pancreatic cancer and head and neck cancers. Additionally, high expression of SCAND2 RNA was correlated with better prognoses of lung adenocarcinoma and sarcoma. These data suggest that the stress-inducible SCAN-TFs can function as a feedback system, suppressing excessive stress response and inhibiting cancers. - Source: PubMed
Publication date: 2023/03/08
Sheta MonaYoshida KunihiroKanemoto HidekaCalderwood Stuart KEguchi Takanori - Epithelial-mesenchymal transition (EMT) is a reversible cellular program that transiently places epithelial (E) cells into pseudo-mesenchymal (M) cell states. The malignant progression and resistance of many carcinomas depend on EMT activation, partial EMT, or hybrid E/M status in neoplastic cells. EMT is activated by tumor microenvironmental TGFβ signal and EMT-inducing transcription factors, such as ZEB1/2, in tumor cells. However, reverse EMT factors are less studied. We demonstrate that prostate epithelial transcription factor SCAND1 can reverse the cancer cell mesenchymal and hybrid E/M phenotypes to a more epithelial, less invasive status and inhibit their proliferation and migration in DU-145 prostate cancer cells. SCAND1 is a SCAN domain-containing protein and hetero-oligomerizes with SCAN-zinc finger transcription factors, such as MZF1, for accessing DNA and the transcriptional co-repression of target genes. We found that SCAND1 expression correlated with maintaining epithelial features, whereas the loss of SCAND1 was associated with mesenchymal phenotypes of tumor cells. SCAND1 and MZF1 were mutually inducible and coordinately included in chromatin with hetero-chromatin protein HP1γ. The overexpression of SCAND1 reversed hybrid E/M status into an epithelial phenotype with E-cadherin and β-catenin relocation. Consistently, the co-expression analysis in TCGA PanCancer Atlas revealed that SCAND1 and MZF1 expression was negatively correlated with EMT driver genes, including CTNNB1, ZEB1, ZEB2 and TGFBRs, in prostate adenocarcinoma specimens. In addition, SCAND1 overexpression suppressed tumor cell proliferation by reducing the MAP3K-MEK-ERK signaling pathway. Of note, in a mouse tumor xenograft model, SCAND1 overexpression significantly reduced Ki-67(+) and Vimentin(+) tumor cells and inhibited migration and lymph node metastasis of prostate cancer. Kaplan-Meier analysis showed high expression of SCAND1 and MZF1 to correlate with better prognoses in pancreatic cancer and head and neck cancers, although with poorer prognosis in kidney cancer. Overall, these data suggest that SCAND1 induces expression and coordinated heterochromatin-binding of MZF1 to reverse the hybrid E/M status into an epithelial phenotype and, inhibits tumor cell proliferation, migration, and metastasis, potentially by repressing the gene expression of EMT drivers and the MAP3K-MEK-ERK signaling pathway. - Source: PubMed
Publication date: 2022/12/10
Eguchi TakanoriCsizmadia EvaKawai HotakaSheta MonaYoshida KunihiroPrince Thomas LWegiel BarbaraCalderwood Stuart K