Ask about this productRelated genes to: LARP1 Blocking Peptide
- Gene:
- LARP1 NIH gene
- Name:
- La ribonucleoprotein domain family member 1
- Previous symbol:
- -
- Synonyms:
- LARP, KIAA0731, MGC19556
- Chromosome:
- 5q33.2
- Locus Type:
- gene with protein product
- Date approved:
- 2005-06-16
- Date modifiied:
- 2015-11-18
Related products to: LARP1 Blocking Peptide
Related articles to: LARP1 Blocking Peptide
- Chemoresistance remains a major obstacle in managing cholangiocarcinoma (CCA). The cannabis plant contains several phytocannabinoids, including cannabidiol (CBD), cannabigerol (CBG), and cannabinol (CBN), which exhibit anticancer properties. However, to the best of our knowledge, their effects on CCA have not been previously investigated. This study aimed to explore the molecular mechanisms underlying the anticancer effects of CBD, CBG, and CBN in CCA cells. KKU-100 and KKU-452 cells were treated with varying concentrations of CBD, CBG, and CBN for 24 and 48 h. Cytotoxicity was assessed using the MTT assay, and half maximal inhibitory concentration (IC) values were calculated. KKU 452 cells were further analyzed for apoptosis, mitochondrial membrane potential (MMP), and Ki67 expression using flow cytometry. Proteomics profiling was performed to compare the effect of these cannabinoids with those of gefitinib and cisplatin. Monotherapy with CBD, CBG, or CBN induced dose-dependent cytotoxicity at 24 and 48 h with lower IC values than those of cisplatin and comparable efficacy to that of gefitinib. At low doses, CBD, CBG, and CBN induced early apoptosis, while higher doses triggered late apoptosis. MMP loss increased by 2.5-, 4.9-, and 1.7-fold, respectively, after 6 h. Ki67, highly expressed in KKU-452 cells (Ki67-positive ratio = 3.16 ± 0.16), was significantly reduced after the cannabinoid treatment, with Ki67-positive ratios of 0.38 ± 0.22, 0.38 ± 0.13, and 0.32 ± 0.23 for CBD, CBG, and CBN, respectively. Proteomics analysis identified 2781 proteins affected by CBD, CBG, CBN, cisplatin, and gefitinib. All three cannabinoids downregulated key upstream regulatory proteins (LARP1, TFEB, and BCR). Similar patterns of LARP1 and TFEB downregulation were also observed with cisplatin and gefitinib. CBN showed the closest similarity to cisplatin, followed by gefitinib, by targeting CDK4/6 and PCGEM1 proteins. CBD and CBG exhibited the greatest similarity to each other, also influencing MASTL expression. CBD, CBG, and CBN exhibit potential anticancer activity in CCA by suppressing proliferation, reducing Ki67 expression, and inducing apoptosis through MMP disruption. The identification of shared molecular targets, including LARP1 and TFEB, provides new mechanistic insight and supports the potential development of cannabinoid-based therapeutic strategies for cholangiocarcinoma. - Source: PubMed
Publication date: 2026/07/13
Laprom SahaphumShuntawiwat BoonyaRattanacheeworn PunyabhornJaisin YamarateeChoowongkomon KiattaweeSamatiwat Papavee - - Source: PubMed
Publication date: 2026/07/20
Curdy NicolasTopisirovic Ivan - Epilepsy results from an imbalance between excitation and inhibition of neurons, with 30-40% of cases being temporal lobe epilepsy (TLE). This study aimed to prioritize autophagy-related genes and explore their potential links to immune features in human hippocampal tissue of TLE. Two hippocampal transcriptomic datasets (GSE202101 and GSE11882) were analyzed to identify autophagy-related differentially expressed genes (ARDEGs). Functional enrichment, regulatory network, and immune cell infiltration analyses were performed. LASSO regression and consensus clustering were applied. Exploratory assessment of the candidate gene signature was conducted in an independent dataset (GSE256068). Immunohistochemistry (IHC) on clinical specimens assessed protein expression of candidate signature genes. An eight‑gene candidate signature was derived, and subsequent PPI network analysis revealed LARP1, EIF4G1, and TSC2 as hub genes among them. Exploratory assessment in an independent dataset partially replicated the expression patterns of PYCARD, EIF4G1, and TSC2, whereas LARP1 showed an opposite expression trend; overall model performance remained modest. Increased activated mast cells were observed in TLE samples, while higher levels of plasma cells, CD8⁺ T cells, and regulatory T cells were observed in controls. Two exploratory clusters with distinct immune correlation patterns were identified. IHC showed upregulation of ABL1, TSC2, and SPP1 protein levels in TLE tissue. This study prioritizes a set of autophagy-related candidate genes in human hippocampal tissue and provides an exploratory framework linking them to local immune features in TLE. Further validation in larger independent cohorts is warranted before any clinical interpretation. - Source: PubMed
Publication date: 2026/07/14
Liu JingWang YitingSheng DandanLi XinruYazgulyyeva BibiXiao BoLiu Weiping - Worldwide, breast cancer (BRCA) remains the most common cancer among women. Identifying novel biomarkers that not only predict prognosis but also inform therapeutic response is urgently needed. La-related protein 1 (), an RNA-binding protein and downstream effector of the PI3K/AKT/mTOR pathway, is related to multiple forms of cancer, though its impact on BRCA is not well understood. - Source: PubMed
Publication date: 2026/06/16
Ye YangtianYin HongShen XiangyuLi FuchengLiu LuyaoSun Dao - Tumor initiation requires the integration of oncogenic signals with environmental cues to enable anabolic growth. MYC is central to tumorigenesis, with its deregulation observed in over 60% of human cancers. Oncogenic MYC profoundly rewires transcription, enabling cells to bypass cell cycle checkpoints and reset metabolism. A cornerstone of this rewiring is the upregulation of biomass-producing pathways, particularly ribosome biogenesis. How and when MYC's oncogenic program is translationally executed-either immediately or until a favorable metabolic context emerges-remains a central unanswered question in tumor initiation, limiting our understanding of tumor latency and early intervention. Here, we identify LARP1 as a critical effector of MYC-driven transformation, connecting MYC oncogenic activity with mTOR signaling. Mechanistically, MYC represses miR-26a/b, relieving posttranscriptional repression of LARP1 and leading to its upregulation. LARP1 associates with the translational machinery, loading it with the anabolic translatome induced by MYC in a translationally poised state. Upon permissive mTOR signaling, and dependent on the phosphorylation of LARP1 at serines 689 and 697, this program is rapidly translated, fueling the biosynthetic processes essential for tumor development. Importantly, genetic deletion of LARP1 or pharmacological mTOR inhibition completely abrogates tumor initiation in a genetically engineered colorectal organoid model of MYC-driven tumorigenesis. This underscores the physiological relevance of this two-step mechanism in which LARP1 bridges the anabolic translatome primed by MYC with its metabolic execution controlled by mTOR. By temporally uncoupling transformation from metabolic permissiveness, this mechanism defines a critical checkpoint in early tumorigenesis, revealing a potential vulnerability for intercepting MYC-driven cancer before biomass expansion. - Source: PubMed
Publication date: 2026/06/12
Fuentes PedroIannizzotto FlaviaBattaglia ElisaBalzamo ChiaraTola CarlaForcada BertaBosch-I-Crespo PauMorón-Duran Francisco DFrank Brandon EMartínez-Herráez CarolinaMastora ZoiManfili-Marinho GabriellaTauler AlbertSantos CristinaSalazar RamónGentilella Antonio