Ask about this productRelated genes to: SPRR3 Blocking Peptide
- Gene:
- SPRR3 NIH gene
- Name:
- small proline rich protein 3
- Previous symbol:
- -
- Synonyms:
- -
- Chromosome:
- 1q21.3
- Locus Type:
- gene with protein product
- Date approved:
- 1993-01-20
- Date modifiied:
- 2016-10-05
Related products to: SPRR3 Blocking Peptide
Related articles to: SPRR3 Blocking Peptide
- Clarification of the molecular mechanism of malignant tumor progression, identification of the key signaling pathways and molecules involved in the processes of invasion and metastasis, and identification of new targets and strategies for effective tumor treatment are extremely important for scientific research and clinical application prospects. - Source: PubMed
Publication date: 2026/04/03
Shi Yuan-Xiang - Return to sport (RTS) after anterior cruciate ligament reconstruction (ACLR) remains a critical issue in sports medicine. Despite improvements in rehabilitation, many patients fail to return to their preinjury level of activity. Previous studies have primarily focused on clinical and biomechanical factors that influence RTS; however, the impact of intrinsic physiological changes, particularly urinary proteomic profiles, has not yet been fully explored. This study aimed to identify potential urinary protein biomarkers associated with RTS in ACLR patients. - Source: PubMed
Publication date: 2026/01/10
Zhu TingLi YuanyuanZhao YingqiGong YaweiZhou JingbinXu Xin - Cervical cancer remains a significant cause of cancer-related mortality among women, particularly in low- and middle-income countries. High-throughput technologies, such as microarrays, have facilitated the comprehensive analysis of gene expression profiles in cervical cancer, enabling the identification of key differentially expressed genes (DEGs) involved in its pathogenesis. The publicly available microarray datasets, including GSE39001, GSE9750, GSE7803, GSE6791, GSE63514, and GSE52903 in combination with bioinformatics database predictions, were used to identify differential expression genes, potential biomarkers, and therapeutic targets for cervical cancer; additionally, we undertook bioinformatic analysis to determine gene ontology and possible miRNA targets related to our DEGs. Our analysis revealed several DEGs significantly associated with cervical cancer progression, such as cell death, regulation of DNA replication, protein binding processes, and transcription factors. The most relevant transcription factors (TFs) identified were SP1, ELF3, E2F1, TP53, RELA, HDAC, and FOXM1. Importantly, the DEGs with more important changes were 11 coding genes that were upregulated () and 14 that were downregulated (), which were associated with cervical cancer. Interestingly, hub proteins KIF4A, NUSAP1, BUB1B, CEP55, DLGAP5, NCAPG, CDK1, MELK, KIF11, and KIF20A were found to be potentially regulated by several miRNAs, including miR-107, miR-124-3p, miR-147a, miR-16-5p, miR-34a-5p, miR-34c-5p, miR-126-3p, miR-10b-5p, miR-23b-3p, miR-200b-3p, miR-138-5p, miR-203a-3p, miR-214-3p, and let-7b-5p. The relationship between these genes highlights their potential as candidate biomarkers for further research in treatment, diagnosis, and prognosis. - Source: PubMed
Publication date: 2025/12/26
Alvarado-Camacho Diego ArmandoCastillo-Velázquez RicardoGranados-López Angelica JudithHernández-López HiramLópez-Hernández YamiléGutiérrez-Hernández RosalindaVarela-Silva José AntonioReyes-Estrada Claudia AraceliSolorio-Alvarado Cesar RogelioSánchez-Rodríguez Sergio HugoGarcía-López David AlejandroLópez Jesús Adrián - SPRR3 is a small, proline-rich protein that promotes cell proliferation. Overexpressed SPRR3 is associated with cancer and regulates AKT phosphorylation at serine 473. However, the specific cellular mechanisms by which SPRR3 drives proliferation are not fully understood. Using a genome-wide siRNA screen in MCF10A breast epithelial cells for decreased nucleolar number, we identified SPRR3 as a novel regulator of ribosome biogenesis. We used siRNA to deplete SPRR3 and found that it is required for transcription of the pre-ribosomal RNA (pre-rRNA), the earliest step in ribosome biogenesis. Furthermore, this reduction in pre-rRNA transcription triggers the nucleolar stress response (increased TP53 protein and CDKN1A mRNA levels) in both MCF10A cells and A549 lung carcinoma cells. Finally, SPRR3 depletion reduces AKT phosphorylation in both cell lines and correlates with lower levels of the RNAPI catalytic subunit POLR1A. In sum, we establish a new role for the non-nucleolar protein SPRR3 in ribosome biogenesis, specifically pre-rRNA transcription, via its ability to facilitate phosphorylation of AKT. - Source: PubMed
Publication date: 2026/01/07
Sutton Emily CBryant Carson JGbenoba Janina I SLawrence Isabella RBaserga Susan J - Breast cancer is the most common tumor type in women and with apparent genetic predisposition. Recent genome-wide association study suggests that rs527616 is significantly associated with this disease. Analysis on 1000 genomes project data suggests that additional four SNPs, rs604702, rs1667550, rs521667, and rs675150, are in nearly complete linkage disequilibrium with rs527616. However, the causal SNP and the mechanism for this association still remain unclear. Reporter gene assay indicates that the causal SNP might be not rs527616 but rs604702. BARX2 (BARX homeobox 2) is identified to bind the surrounding region of rs604702 and binding affinity difference between alleles is compared. The enhancer containing rs604702 can interact with PCAT18 (prostate cancer associated transcript 18) promoter. Knockdown of PCAT18 can significantly decrease SPRR3 (small proline rich protein 3) expression and breast cell ability of proliferation, migration, wound healing, and colony formation, which verifies that PCAT18 is an oncogene for breast cancer. Transfection of miR-759 inhibitor can rescue abovementioned effect, thus validating that the effect of PCAT18 on breast cancer is through interacting with this miRNA. Knock-out of rs604702 surrounding region by CRISPR/Cas9 can significantly decrease PCAT18 and SPRR3 expression and further breast cell ability of proliferation, migration, wound healing, and colony formation. Our effort identifies a novel mechanism by which the genetic variation in this locus can influence breast cancer susceptibility. - Source: PubMed
Publication date: 2025/11/05
Zhang Xin-XinLi Ya-JieZhou Xi-TingSong Hong-LiGuo HaoLi Hai-YanTian Li-YuanSun Chang