STMN1 _ Stathmin 1
- Known as:
- STMN1 _ Stathmin 1
- Catalog number:
- Y213493
- Product Quantity:
- 200ul
- Category:
- -
- Supplier:
- ABM
- Gene target:
- STMN1 _ Stathmin 1
Related genes to: STMN1 _ Stathmin 1
- Gene:
- STMN1 NIH gene
- Name:
- stathmin 1
- Previous symbol:
- LAP18, C1orf215
- Synonyms:
- SMN, OP18, PR22, PP19, PP17, Lag, FLJ32206
- Chromosome:
- 1p36.11
- Locus Type:
- gene with protein product
- Date approved:
- 1990-12-17
- Date modifiied:
- 2014-11-19
Related products to: STMN1 _ Stathmin 1
Related articles to: STMN1 _ Stathmin 1
- Oral squamous cell carcinoma (OSCC) is a common malignant tumor in the head and neck region and clinically characterized by relatively high invasiveness and a propensity for metastasis. Patients generally exhibit nonsatisfactory prognosis. Beyond the classical endothelium-dependent angiogenesis pathway, vasculogenic mimicry (VM), a nonclassical blood supply mechanism whereby tumor cells themselves form microcirculatory conduits, plays a significant role in tumor progression. However, the regulatory mechanism of VM formation remains to be fully understood. U2AF homologous motif kinase 1 (UHMK1) is a regulatory protein possessing serine/threonine kinase activity and RNA-binding capability and was found to be overexpressed in OSCC tissues in our previous research. The present study aimed to explore the association between UHMK1 expression in OSCC and VM formation and elucidate the potential molecular mechanisms by which UHMK1 regulates VM development. Immunohistochemistry (IHC) results demonstrated that UHMK1 upregulation in OSCC was significantly correlated with VM structure, and both were associated with poor clinical outcomes and shortened patient survival time. In vitro experiments revealed that UHMK1 knockdown markedly suppressed VM formation in OSCC cells. Bioinformatics prediction and co-immunoprecipitation (co-IP) assays confirmed the interaction between UHMK1 and stathmin1 (STMN1). Further investigations indicated that UHMK1 stabilized STMN1 protein expression by inhibiting its ubiquitin-proteasome degradation pathway, and these two might jointly activate the PI3K/AKT/mTOR signaling pathway to regulate VM formation. The current study revealed the key role of UHMK1-STMN1 in coregulating VM formation in OSCC, providing new insights into the tumor microenvironment and identifying potential targets for anti-angiogenic therapy. - Source: PubMed
Publication date: 2026/04/09
Guo YanFeng YuanyongNi XiangningZhang XuanFang XiaoLi TongtongWang Ning - Immune checkpoint inhibitors (ICIs) targeted PD-1/PD-L1 axis generate immune-related adverse events such as myocarditis, limiting their clinical application. Herein, we tried to explore the potential mechanism of ICIs-induced myocarditis. We performed single-cell RNA sequencing of heart tissues and peripheral blood mononuclear cells (PBMC) collected from mice with or without a relative low dose of PD-1/PD-L1 inhibitor (BMS-1) treatment. Compared with PBS treatment, BMS-1 treatment increased T, B, NK cells, and neutrophils but decreased macrophages in the heart. Four T cell subclusters in the heart were identified, including Treg, LEF1+CD4+ T, CCL5+CD8+ T, and STMN1+CD8+ T cells. The BMS-1-heart exhibited increased CCL5+CD8+ T cells depicted by elevated Nkg7 and Ccl5 gene expression compared with the PBS-heart. The number of macrophages declined but revealed inflammatory activity in the BMS-1-heart. Interestingly, CCR5, a receptor for CCL5 expressed in both CCR2- resident and CCR2+ recruit macrophages in the heart, was upregulated by the BMS-1 treatment. In addition, fibroblasts, not endothelial cells, showed an inflammatory activation state. Last, we identified increased CCL5+CD8+ T cells in the BMS-1-PBMC. Immunofluorescence staining also confirmed significantly elevated CCL5+CD8+ T cells in the BMS-1-heart than that of PBS-heart. BMS-1 seems to recruit circulating CCL5+CD8+ T cells to the heart, which further interact with CCR5+ macrophages, resulting in fibroblast activation. The CCL5/CCR5 axis and circulating CCL5+CD8+ T cells may be potential therapeutic/diagnostic strategies for ICIs-induced myocarditis. - Source: PubMed
Yan ChenYe CongWang Kai-XuanLi Xin-RanJiang Zhi-TingBian Si-JiaNie HanZhu Yu-HuaDu HongLuo Lan - Pituitary tumors, as common intracranial neoplasms, present challenges in clinical management because of high postoperative recurrence rate, drug resistance and pronounced side effects. Astragaloside IV (AS‑IV), the primary active component of the traditional Chinese herb , has antitumor activity in numerous types of cancer. However, its effects and mechanisms in pituitary tumors remain unclear. The present study aimed to investigate the effects of AS‑IV on proliferation and apoptosis of pituitary tumor cells and to elucidate its molecular mechanisms. Cell Counting Kit‑8 (CCK‑8), TUNEL, EdU, immunohistochemistry (IHC), and Western blotting, among others, showed that AS‑IV significantly suppressed the viability of the rat pituitary tumor cell lines GH3 and MMQ in a concentration‑ and time‑dependent manner while inducing apoptosis. Tubulin β4B Class IVb (TUBB4B) was highly expressed in pituitary tumor tissue and its overexpression promoted cell proliferation while inhibiting apoptosis. AS‑IV bound TUBB4B with high affinity, forming a stable complex. TUBB4B regulation influenced pituitary tumor cell sensitivity to AS‑IV, with AS‑IV demonstrating enhanced antitumor efficacy in TUBB4B‑overexpressing tumors. TUBB4B activated the ERK/MAPK signaling pathway by upregulating Stathmin 1 (STMN1) expression, which promoted G1/S phase transition. The ERK‑specific inhibitor U0126 reversed this pro-proliferative effect. To the best of our knowledge, the present study is the first to reveal that AS‑IV inhibits pituitary tumor proliferation and promotes apoptosis by targeting TUBB4B to regulate the STMN1‑ERK signaling axis, providing a novel theoretical basis and potential strategies for traditional Chinese medicine treatment and molecular targeted research on pituitary tumors. - Source: PubMed
Publication date: 2026/04/03
Li JialeQu YufeiZhang WengeYang ZexuZeng YangdongXu JishengXie KuncenLiu Qi - Lung cancer is an aggressive malignancy associated with a rapid progression and poor prognosis, for which immunotherapy only exhibits modest efficacy in most patients. In lung cancer, high lactate is associated with a low immunotherapy response and shortened survival; however, causal lactylation‑related genes remain to be elucidated. In the present study, candidate genes were screened using Mendelian randomization (MR) analysis, with expression quantitative trait loci data and genome‑wide association study summary statistics used as analytical resources. A total of 46 lactylation‑related genes were included in the MR analysis, and multiple testing correction was performed using the false discovery rate (FDR) and Bonferroni methods to control the false‑positive risk. MR identified three core genes [platelet‑type phosphofructokinase; SWI/SNF related, matrix associated, actin dependent regulator of chromatin, subfamily a, member 4; and stathmin 1 ()]. Among these genes, only was significantly associated with increased lung cancer risk (inverse variance weighting original P=0.005, FDR‑corrected P=0.014995, Bonferroni‑corrected P=0.014995, odds ratio=1.741, 95% confidence interval: 1.182‑2.564), with robust results confirmed by heterogeneity/pleiotropy/sensitivity analyses. Subsequently, transcriptomic analysis was conducted to assess STMN1 expression in lung cancer tissues and its association with patient survival. (cell proliferation, migration, invasion and apoptosis assays) and in vivo experiments (murine tumor models) were also conducted to explore the function of . exhibited upregulation in lung cancer tissues, and was associated with a shorter survival, reduced antitumor immune cell infiltration and an immunosuppressive tumor microenvironment (TME) phenotype. knockdown inhibited lung cancer malignancy both and , and modulated key markers, whereas its overexpression exhibited the opposite effects. Additionally, promoted global histone lactylation and histone H3 lysine 18 lactylation in lung cancer cells, establishing a direct functional link between and the lactylation pathway. In conclusion, STMN1 is a lactylation‑related causal oncogene in lung cancer, driving progression via malignant phenotypes, and its high expression is associated with an immunosuppressive TME that may synergistically facilitate tumor progression. Therefore, may be considered a novel target for lung cancer therapy. - Source: PubMed
Publication date: 2026/04/03
Cai YifanZhong YuchengWang HonglinZhu ShuangHuang FangZhang QiuyueHu Shaobo - Lactylation, a novel post-translational modification driven by lactate accumulation, has been implicated in neuroinflammation and metabolic stress. However, its causal relevance to ischemic stroke (IS) and its subtypes—large artery stroke (LAS), cardioembolic stroke (CES), and small vessel stroke (SVS)—remains unknown. - Source: PubMed
Publication date: 2026/03/24
Kan JiuxuHong YongMin RuoxinZhang BowenWang Hong