Ask about this productRelated genes to: LATS1 antibody
- Gene:
- LATS1 NIH gene
- Name:
- large tumor suppressor kinase 1
- Previous symbol:
- -
- Synonyms:
- WARTS
- Chromosome:
- 6q25.1
- Locus Type:
- gene with protein product
- Date approved:
- 1999-02-18
- Date modifiied:
- 2014-11-19
Related products to: LATS1 antibody
Related articles to: LATS1 antibody
- The Hippo signalling pathway has emerged as an important regulator of host-virus interactions, linking antiviral immunity, viral replication, inflammation, and tissue remodelling. Recent studies show that upstream Hippo kinases such as MST1/2 and LATS1/2 often support antiviral responses, whereas YAP and TAZ can suppress innate immune signalling and may be exploited by viruses to promote infection. However, these effects are highly context dependent, varying according to viral species, cell type, infection stage, interferon signalling, inflammatory cues, and tissue damage. This short review summarises current evidence for Hippo-virus crosstalk and highlights how this pathway may shape both acute antiviral defence and longer-term pathological remodelling. We also discuss therapeutic opportunities and challenges, emphasising that targeting Hippo signalling requires caution because of its dual roles in antiviral immunity and tissue repair. - Source: PubMed
Publication date: 2026/06/11
Bahrami AidaWalter CherylArdestani Amin - Neoadjuvant chemotherapy (NAC) is a key component of the standard treatment regimen for patients with advanced esophageal squamous cell carcinoma (ESCC); however, a substantial proportion of patients fail to benefit from NAC because of intrinsic or acquired chemoresistance, leading to disease progression. Aberrant promoter methylation of tumor suppressor genes has been implicated in the diminished chemotherapy response in patients with ESCC. In this study, we show that hypermethylation of the CpG island of the T-box Transcription Factor 1 (TBX1) promoter is frequently associated with nonresponse to NAC in patients with ESCC. Functional experiments indicate that TBX1 suppresses ESCC cell proliferation, induces apoptosis, and increases cisplatin sensitivity. Mechanistically, TBX1 activates the Hippo signaling pathway through two complementary mechanisms: transcriptional upregulation of MST1 and LATS1 and inhibition of F-actin polymerization. Restoration of TBX1 expression enhances chemosensitivity and reduces tumor growth in vivo. Collectively, our findings suggest that TBX1 promoter hypermethylation has the potential to serve as a predictive biomarker of the NAC response in ESCC and define an epigenetic mechanism in which TBX1 silencing contributes to chemoresistance through impairment of Hippo pathway activation. These results suggest that modulating TBX1 expression and Hippo pathway activity represents a potential therapeutic strategy for overcoming chemoresistance in ESCC. - Source: PubMed
Publication date: 2026/06/09
Xu ZhongMa GangShen YingTan LiSun XuejuanPeng LeiPeng WeiyanYe Lin - Keratoconus (KC) is an adolescent-onset vision-impairing corneal disorder with incompletely elucidated pathogenesis. This study aims to elucidate the regulatory role of NEDD8 in the Hippo-YAP signaling pathway and its influence on the corneal pathology, thereby providing a theoretical basis for mechanistic studies and targeted therapy of KC. - Source: PubMed
Qu JunpengZhang XiaowenWei ChaoYu HuiminDou ShengqianGao Hua - Solamargine is a natural compound derived from the traditional Chinese medicinal plant , and exhibits a variety of biological activities, including anti-inflammatory, antimalarial, pro-apoptotic, analgesic, and antitumor effects. However, the role of solamargine in liver fibrosis remains unclear. This study aims to investigate the anti-fibrotic effects and potential mechanisms of solamargine using human hepatic stellate cells (LX-2 cells) and a carbon tetrachloride (CCl)-induced mouse model of liver fibrosis. - Source: PubMed
Huang RuihuaAli Alshami Mohammed Abdulaziz YahyaZhu XiaoyunHu Changping - Gynecologic cancers (GCs), including ovarian, cervical, and endometrial cancers, represent a substantial global health burden, characterized by high rates of recurrence, therapeutic resistance, and metastatic dissemination. Tumor dormancy-a state in which disseminated tumor cells (DTCs) persist in a non-proliferative, quiescent phase, thereby evading conventional therapies and immune surveillance-constitutes a critical yet often underestimated driver of these clinical challenges. This comprehensive review systematically integrates the multifaceted roles and current research landscape of dormant tumor cells in gynecologic malignancies. The core innovation lies in a three-level analytical framework that examines dormancy through intrinsic molecular switches, extrinsic microenvironmental remodeling, and cross-cancer type comparisons. Specifically, the mechanisms governing dormancy initiation, maintenance, and reactivation are delineated for cervical, ovarian, and endometrial cancers. Several key conclusions emerge from this synthesis. Common regulatory hubs across gynecologic cancers include hypoxic conditions, cell-cycle regulators such as the DREAM complex, stemness-associated pathways exemplified by the HIF-1α/PLD2 axis, and stromal cell interactions, notably cancer-associated fibroblast-extracellular matrix crosstalk. Dormant cells further orchestrate sophisticated immune evasion strategies, including downregulation of major histocompatibility complex class I and upregulation of immune checkpoint molecules, thereby establishing a reservoir of drug-tolerant persister cells that drive post-treatment relapse and acquired resistance. Notably, substantial heterogeneity exists across different gynecologic cancer types: ovarian cancer engages the most diverse repertoire of dormancy-related pathways, while uterine sarcoma remains a conspicuous research gap. Collectively, this review establishes the dormant tumor cell reservoir as a promising therapeutic target to prevent recurrence and overcome therapy resistance. Specific actionable targets-including Dyrk1A, PLD2, LATS1/2, and Egfl6-are proposed, providing a theoretical foundation for the development of novel diagnostic tools and therapeutic strategies aimed at improving long-term outcomes for patients with gynecologic malignancies. - Source: PubMed
Publication date: 2026/05/15
Fu AizhenMa ZhenZou KaiWu FeiyuanZou Xinxin