CEA-Induced PI3K/AKT Pathway Activation through the Binding of CEA to KRT1 Contributes to Oxaliplatin Resistance in Gastric Cancer DOI
Yifan Chen,

Yulong Mi,

Song Tan

и другие.

Drug Resistance Updates, Год журнала: 2024, Номер 78, С. 101179 - 101179

Опубликована: Дек. 3, 2024

Язык: Английский

Fungi, immunosenescence and cancer DOI Creative Commons
Bin Xu,

Zan Luo,

Xing Niu

и другие.

Seminars in Cancer Biology, Год журнала: 2025, Номер 109, С. 67 - 82

Опубликована: Янв. 7, 2025

Язык: Английский

Процитировано

4

T cell exhaustion and senescence for ovarian cancer immunotherapy DOI
Jiao Zhao,

Zhongmiao Wang,

Yingying Tian

и другие.

Seminars in Cancer Biology, Год журнала: 2024, Номер 104-105, С. 1 - 15

Опубликована: Июль 18, 2024

Язык: Английский

Процитировано

9

RGS5+ lymphatic endothelial cells facilitate metastasis and acquired drug resistance of breast cancer through oxidative stress-sensing mechanism DOI
Caixin Qiu,

Chaoyi Tang,

Yujun Tang

и другие.

Drug Resistance Updates, Год журнала: 2024, Номер 77, С. 101149 - 101149

Опубликована: Сен. 6, 2024

Язык: Английский

Процитировано

9

YTHDF2-mediated m6A modification of ONECUT2 promotes stemness and oxaliplatin resistance in gastric cancer through transcriptionally activating TFPI DOI

Xingdi Fan,

Fangyi Han,

Haocheng Wang

и другие.

Drug Resistance Updates, Год журнала: 2025, Номер 79, С. 101200 - 101200

Опубликована: Янв. 2, 2025

Язык: Английский

Процитировано

1

Nanozyme-based synergistic therapeutic strategies against tumors DOI
Ye Zhang, Ning Zhang, Shouping Gong

и другие.

Drug Discovery Today, Год журнала: 2025, Номер unknown, С. 104292 - 104292

Опубликована: Янв. 1, 2025

Язык: Английский

Процитировано

1

A distinct subset of urothelial cells with enhanced EMT features promotes chemotherapy resistance and cancer recurrence by increasing COL4A1-ITGB1 mediated angiogenesis DOI Creative Commons
Jinan Guo,

Xiaoshi Ma,

Dongcheng Liu

и другие.

Drug Resistance Updates, Год журнала: 2024, Номер 76, С. 101116 - 101116

Опубликована: Июль 3, 2024

Drug resistance and tumor recurrence remain clinical challenges in the treatment of urothelial carcinoma (UC). However, underlying mechanism is not fully understood. Here, we performed single-cell RNA sequencing identified a subset cells with epithelial-mesenchymal transition (EMT) features (EMT-UC), which significantly correlated chemotherapy cancer recurrence. To validate significance EMT-UC, constructed EMT-UC like by introducing overexpression two markers, Zinc Finger E-Box Binding Homeobox 1 (ZEB1) Desmin (DES), examined their histological distribution characteristics malignant phenotypes. were mainly enriched UC tissues from patients adverse prognosis exhibited elevated EMT, migration gemcitabine tolerance vitro. was specifically tumorous tissues, certain proportion them also adjacent normal tissues. Tumorous highly expressed genes involved behaviors prognosis. Additionally, associated remodeled microenvironment (TME), high angiogenic immunosuppressive potentials compared counterparts. Furthermore, specific interaction COL4A1 ITGB1 to be endothelial component. Targeting antibodies suppressed angiogenesis alleviated UC. Overall, our findings demonstrated that driven force mediated COL4A1-ITGB1 interaction, providing potential target for future treatment.

Язык: Английский

Процитировано

5

The systemic evolutionary theory of the origin of cancer (SETOC): an update DOI Creative Commons
Antonio Mazzocca, Giovanni Ferraro,

Giovanni Misciagna

и другие.

Molecular Medicine, Год журнала: 2025, Номер 31(1)

Опубликована: Янв. 14, 2025

Abstract The Systemic Evolutionary Theory of the Origin Cancer (SETOC) is a recently proposed theory founded on two primary principles: cooperative and endosymbiotic process cell evolution as described by Lynn Margulis, integration complex systems operating in eukaryotic cells, which core concept biology. SETOC proposes that malignant transformation occurs when cells undergo continuous adaptation response to long-term injuries, leading tissue remodeling, chronic inflammation, fibrosis, ultimately cancer. This involves maladaptive response, wherein 'endosymbiotic contract’ between nuclear-cytoplasmic system (derived from primordial archaeal cell) mitochondrial α-proteobacterium) gradually breaks down. leads uncoordinated behaviors functions transformed cells. decoupling cellular subsystems causes acquire phenotypic characteristics analogous those unicellular organisms, well certain biological features embryonic development are normally suppressed. These adaptive changes enable cancer survive harsh tumor microenvironment characterized low oxygen concentrations, inadequate nutrients, increased catabolic waste, acidity. De-endosymbiosis reprograms sequential metabolic glycolysis, TCA cycle, oxidative phosphorylation (OxPhos). lactate fermentation (Warburg effect), respiratory chain dysfunction, cycle reversal. Here, we present an updated version incorporates fundamental principles outlined this integrates epistemological approach used develop it.

Язык: Английский

Процитировано

0

Distinct Immunophenotypic Profiles and Neutrophil Heterogeneity in Colorectal Cancer DOI

Minghua Bai,

Yuzhao Jin,

Zihao Jin

и другие.

Cancer Letters, Год журнала: 2025, Номер 616, С. 217570 - 217570

Опубликована: Фев. 22, 2025

Язык: Английский

Процитировано

0

Defeating lethal cancer: Interrupting the ecologic and evolutionary basis of death from malignancy DOI Open Access
Kenneth J. Pienta,

Patrick L. Goodin,

Sarah R. Amend

и другие.

CA A Cancer Journal for Clinicians, Год журнала: 2025, Номер unknown

Опубликована: Март 9, 2025

Despite the advances in cancer prevention, early detection, and treatments, all of which have led to improved survival, globally, there is an increased incidence cancer-related deaths. Although each patient tumor wholly unique, tipping point incurable disease common across patients: dual capacity for cancers metastasize resist systemic treatment. The discovery genetic mutations epigenetic variation that emerges during progression highlights evolutionary ecology principles can be used understand how evolves a lethal phenotype. By applying such eco-evolutionary framework, authors reinterpret our understanding metastatic process as one ecologic invasion define paths evolving therapy resistance. With this understanding, draw from successful strategies optimized strategic interventions with goal altering trajectory cancer. Ultimately, studying, treating using provides opportunity improve lives patients

Язык: Английский

Процитировано

0

Overexpression of ESYT3 improves radioimmune responses through activating cGAS-STING pathway in lung adenocarcinoma DOI Creative Commons

Zan Luo,

Ying Li, Bin Xu

и другие.

Experimental Hematology and Oncology, Год журнала: 2024, Номер 13(1)

Опубликована: Авг. 5, 2024

Abstract Background Radiotherapy can modulate systemic antitumor immunity, while immune status in the tumor microenvironment also influences efficacy of radiotherapy, but relevant molecular mechanisms are poorly understood lung adenocarcinoma (LUAD). Methods In this study, we innovatively proposed a radiotherapy response classification for LUAD, and discovered ESYT3 served as suppressor radioimmune sensitizer. expression was measured both radioresistant radiosensitive LUAD tissues cells. The influence on sensitivity resistance then investigated. Interaction between STING evaluated through multiple immunofluorescent staining coimmunoprecipitation, downstream molecules were further analyzed. vivo models constructed to assess combination treatment overexpression with radiotherapy. Results We found that subtype presented immunosuppressive state activation DNA damage repair pathways than subtype. remarkably attenuated Clinically, low linked radioresistance. Overexpression enabled alleviate radioresistance, sensitize cells induced by irradiation. Mechanically, directly interacted STING, activated cGAS-STING signaling, subsequently increasing generation type I IFNs well chemokines CCL5 CXCL10, thus improving responses. had synergistic anticancer effect vitro vivo. Conclusions summary, confers its improve responses activating cGAS-STING-dependent pathway, providing an alternative therapeutic strategy patients.

Язык: Английский

Процитировано

4