HOM-TES-103 Blocking Peptide
- Known as:
- HOM-TES-103 Blocking Peptide
- Catalog number:
- 33r-6035
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Fitzgerald industries international
- Gene target:
- HOM-TES-103 Blocking Peptide
Related products to: HOM-TES-103 Blocking Peptide
Related articles to: HOM-TES-103 Blocking Peptide
- Aberrant alternative splicing (AS) events have been implicated in cancer progression; however, their role in metastatic renal cell carcinoma (mRCC) remains underexplored. This study aims to identify AS events associated with clinical benefits from immune checkpoint inhibitors and targeted therapies in mRCC. - Source: PubMed
Publication date: 2026/05/05
Govindarajan AmeishHansen NathanielMercier Benjamin DByron Sara AHegde ApurvaGarcia-Mansfield KrystineLeskoske KristinChawla NealMeza LuisZengin ZeynepBarragan-Carillo ReginaEbrahimi HedyehCastro Daniela VDizman NazliHsu JoAnnChehrazi-Raffle AlexanderTripathi AbhishekSalgia Nicholas JPal Sumanta KPirrotte Patrick - Accumulating evidence indicates that mitochondrial dynamics are closely linked to the biological behaviors of tumor cells, with increased mitochondrial fission being recognized as a phenotype that promotes tumor growth. Although intermediate filament family orphan 1 (IFFO1) has been implicated in mitochondrial dynamics, its specific role and molecular mechanisms in regulating mitochondrial fission during breast cancer (BC) progression remain unclear. In this study, analysis of tumor and adjacent normal tissues from 30 BC patients revealed significant downregulation of IFFO1 in tumor tissues, and low IFFO1 expression predicted poor prognosis in patients. In vitro experiments demonstrated that IFFO1 overexpression suppressed the proliferation, invasion, and epithelial-mesenchymal transition (EMT) of BC cells by inhibiting mitochondrial fission and fatty acid synthesis. Mechanistically, IFFO1 interacts with LaminA/C to promote its expression, which subsequently upregulates PGC1α, thereby suppressing mitochondrial fission and fatty acid synthesis in BC cells. Consistent with this mechanism, both LaminA/C and PGC1α were downregulated in BC tissues. Silencing LMNA reversed the inhibitory effects of IFFO1 overexpression on mitochondrial fission and fatty acid synthesis, whereas overexpression of PGC1α effectively counteracted the consequences of LMNA knockdown. In vivo studies confirmed that upregulation of IFFO1 inhibited tumor growth in xenograft models and reduced lung metastasis in a lung metastasis mouse model. These findings underscore the significance of the IFFO1/LaminA/C/PGC1α pathway as a key regulator of mitochondrial fission and fatty acid synthesis during BC progression and highlight its potential as a therapeutic target for breast cancer. - Source: PubMed
Publication date: 2026/03/17
Cai HuaxiaHe Jianjun - Chromosomal translocation (CT) is characterized by incorrect ligation between chromosome fragments when multiple DNA double-strand breaks (DSBs) exist simultaneously. DNA repair, the three-dimensional structure of the nucleoskeleton, and the spatial and temporal movement of DSB ends contribute to CTs. Our earlier research showed that Intermediate Filament Family Orphan 1 (IFFO1) links the nucleoskeleton and non-homologous end joining (NHEJ) to prevent CTs. In this study, we identified the paralog IFFO2, which, together with IFFO1, forms a complex interaction network. We demonstrate that the C-terminus of these IFFOs binds to XRCC4 to facilitate its participation in the NHEJ process. In contrast, their N-termini oversee the building of the nucleoskeleton by connecting with each other and Lamin A/C. Interestingly, IFFO1 and IFFO2 show epistatic effects in suppressing CT by anchoring broken DNA ends and have non-epistatic roles in NHEJ-mediated DSB repair. Our results define an integrated nucleoskeleton composed of IFFO1-IFFO2-Lamin A/C, and reveal its dual functions in genome stability maintenance, the promotion of end-joining, and the suppression of CT. - Source: PubMed
Liu JingyanBai XiuzhenChen XinpengLi BohanZhao HuayuWu JiahuiYe YuanlingYu JiayiYan ZhenxinGuo RongXu DongyiLi Wen - Melanoma exhibited a poor prognosis due to its aggression and heterogeneity. The effect of glutamate metabolism promoting tumor progression on cutaneous melanoma remains unknown. Herein, glutamine metabolism-related genes (GRGs) were identified followed by constructing a prognostic model for melanoma via bioinformatics analysis. - Source: PubMed
Publication date: 2025/08/20
Hu HongyanYang JingMiao JinLi ChenWang CaoRan FengmingZou JieZhang YiZhao LiufangZhao WentaoAi Conghui - The metastasis of lung cancer represents a significant factor contributing to the failure of clinical treatment, and the mechanisms involved are intricate and not yet completely elucidated. Intermediate filaments, which constitute a key element of the cytoskeleton, function not only as diagnostic markers but also play a role in malignant processes, including tumor proliferation, apoptosis, and migration. The intermediate filament IFFO1 is essential for genomic stability, and its expression level serves as a prognostic indicator in various tumors. However, the functional contributions of IFFO1 in tumor progression remain inadequately understood. Our study revealed that IFFO1 is downregulated in lung cancer patients and is correlated with a poorer prognosis. The depletion of IFFO1 led to enhanced tumor proliferation both in vitro and in vivo, as well as increased cellular migration, alterations in the cytoskeleton and modifications in GTPase-mediated signal transduction. Mechanically, IFFO1 was found to interact directly with the GTPase-related scaffold IQGAP3 through the 2 A coiled-coil domain, which was critical for the inhibition of cellular mobility. Moreover, the increased cell migration observed in IFFO1-deficient cells was substantiated as being facilitated by IQGAP3. Finally, IFFO1 was shown to inhibit the association of IQGAP3 with its effector Cdc42 in a dose-dependent manner. Our study demonstrates the multifaceted roles of IFFO1 in lung cancer by modulating the IQGAP3-Cdc42 axis and suggests the potential for identifying tumor targets through the examination of intermediate filament networks and their associated co-factors. - Source: PubMed
Publication date: 2025/07/10
Ye YuanlingShen FanYan MaoliZhan ConghuiLv JiahuaZou MengqinWang ZhifengNing ShaokaiGao YanfeiWu JingxianLi Wen