CT45

Last update 08 May 2025

Basic Info

Synonyms

Cancer/testis antigen family 45

Introduction-

100 Clinical Results associated with CT45

100 Translational Medicine associated with CT45

0 Patents (Medical) associated with CT45

Literatures (Medical) associated with CT45

01 Jun 2025·Colloids and Surfaces B: Biointerfaces

A computer-aided, carrier-free drug delivery system with enhanced cytotoxicity and biocompatibility: A universal model for multifunctional lung cancer therapy

Article

Author: Fu, Xin ; Lai, Yuxin ; Lei, Shizeng ; Zhang, Yingying ; Wang, Ying ; Xu, Wenjing ; Yang, Liyan ; Wang, Zhonglei ; Xiang, Ziling

Erlotinib (ERL) is a first-line targeted therapy for patients with epidermal growth factor receptor (EGFR)-mutant advanced non-small cell lung cancer (NSCLC). However, its effectiveness is hindered by acquired resistance and poor bioavailability. Carrier-free nanodrugs are a research hotspot due to their efficient targeting, high drug loading capacity, and the absence of any excipients. Herein, we report an advanced self-delivery system for multimodal NSCLC therapy using a computer-aided strategy. First, we developed a novel heterodimer, ERL-SS-QM (ERL conjugated with QM-OH-a hydrophobic aggregation-induced emission fluorophore-via a disulfide bond [SS]), which serves as both cargo and carrier material. Self-assembly is driven by multiple noncovalent interactions, including π-π stacking and sulfur bonds. Subsequently, an ERL-SS-QM-based "triadic" drug delivery nanoplatform comprising 21 variants was developed. A case study on ursolic acid (UA)-loaded ERL-SS-QM nanoparticles (named UA@ERL-SS-QM NPs) revealed narrow size distribution, small particle size, and well stabilized (zeta potential = -28.9 mV). The UA@ERL-SS-QM NPs demonstrated concentration-dependent toxicity against targeted A549 cells (IC₅₀ = 4.36 μM), outperforming free monomeric drugs ERL (IC₅₀ = 12.94 μM) and UA (IC₅₀ = 12.21 μM), indicating good efficiency. Conversely, these NPs exhibited minimal cytotoxicity in non-targeted BEAS-2B cells, suggesting favorable biocompatibility. Upon endocytosis and interaction with overexpressed GSH in A549 cells, the disulfide-bond linker is cleaved to release three components: ERL, UA (which downregulates β-catenin/TCF4/CT45A2 signaling pathways, inducing apoptosis in ERL-resistant L858R/T790M mutant cells-a key factor in acquired resistance to ERL treatment), and QM-OH. Hence, this work provides a universal model for multifunctional NSCLC therapy that effectively addresses ERL resistance while enhancing cytotoxicity and biocompatibility.

01 Feb 2025·Molecular Oncology

CT45A1‐mediated MLC2 (MYL9) phosphorylation promotes natural killer cell resistance and outer cell fate in a cell‐in‐cell structure, potentiating the progression of microsatellite instability‐high colorectal cancer

Article

Author: Lin, Yen‐Yu ; Lan, Hsin‐Yi ; Lin, Chun‐Chi ; Huang, Hsiang‐Yueh ; Hwang, Wei‐Lun ; Teng, Hao‐Wei ; Twu, Yuh‐Ching ; Yang, Wen‐Hao ; Lin, Wen‐Chun

Patients with microsatellite instability‐high (MSI‐H) colorectal cancer (CRC) have high tumor mutation burden and tumor immunogenicity, exhibiting a higher response rate to immunotherapy and better survival. However, a portion of MSI‐H CRC patients still experience adverse disease outcomes. We aimed to identify the tumor‐autonomous regulators determining these heterogeneous clinical outcomes. The Cancer Genome Atlas (TCGA) dataset was used to identify regulators in MSI‐H CRC patients with unfavorable outcomes. Stable CRC tumor clones expressing targeted regulators were established to evaluate migratory and stemness properties, immune cell vulnerability, and cell‐in‐cell (CIC) structure formation. RNA‐sequencing (RNA‐seq) was used to identify enriched biological pathways in stable CRC tumor clones. Clinicopathological characterization of formalin‐fixed paraffin‐embedded (FFPE) MSI‐H CRC specimens was performed to explore the underlying mechanisms involved. We showed that cancer/testis antigen family 45 member A1 (CT45A1) expression was upregulated in MSI‐H CRC patients with poor survival outcomes. CT45A1‐expressing microsatellite stable (MSS) CRC cells showed enhanced migratory ability. However, CT45A1‐expressing MSI‐H CRC cells, but not MSS CRC cells, showed higher resistance to natural killer (NK) cell cytotoxicity and served as outer cells in homotypic CIC structures, preventing exogenous or therapeutic antibody access to inner CRC cells. Inactivating RHO‐ROCK/MLCK‐MLC2 signaling with small‐molecule inhibitors or short‐hairpin RNAs (shRNAs) targeting myosin light chain kinase (MYLK) abolished NK cell resistance and reduced the outer cell fate of CT45A1‐expressing MSI‐H CRC cells. In MSI‐H CRC patients, CT45A1‐positive tumors exhibited increased MLC2 phosphorylation, increased outer cell fate, and decreased survival. We demonstrated that CT45A1 potentiates the advanced progression of MSI‐H CRC, and targeting MLC2 phosphorylation may enhance immunotherapy efficacy in CT45A1‐positive MSI‐H CRC patients.

01 Dec 2024·Biochimica et Biophysica Acta (BBA) - Gene Regulatory Mechanisms

Machine learning based analysis of single-cell data reveals evidence of subject-specific single-cell gene expression profiles in acute myeloid leukaemia patients and healthy controls

Article

Author: Chrysostomou, Andreas ; Furlan, Cristina ; Saccenti, Edoardo

Acute Myeloid Leukaemia (AML) is characterized by uncontrolled growth of immature myeloid cells, disrupting normal blood production. Treatment typically involves chemotherapy, targeted therapy, and stem cell transplantation but many patients develop chemoresistance, leading to poor outcomes due to the disease's high heterogeneity. In this study, we used publicly available single-cell RNA sequencing data and machine learning to classify AML patients and healthy, monocytes, dendritic and progenitor cells population. We found that gene expression profiles of AML patients and healthy controls can be classified at the individual level with high accuracy (>70 %) when using progenitor cells, suggesting the existence of subject-specific single cell transcriptomics profiles. The analysis also revealed molecular determinants of patient heterogeneity (e.g. TPSD1, CT45A1, and GABRA4) which could support new strategies for patient stratification and personalized treatment in leukaemia.

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CT45

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