Long non-coding RNA/epithelial-mesenchymal transition axis in human cancers: Tumorigenesis, chemoresistance, and radioresistance DOI
Mehrdad Hashemi, Shima Hajimazdarany, Chakrabhavi Dhananjaya Mohan

et al.

Pharmacological Research, Journal Year: 2022, Volume and Issue: 186, P. 106535 - 106535

Published: Nov. 2, 2022

Language: Английский

Triple-Negative Breast Cancer Progression and Drug Resistance in the Context of Epithelial–Mesenchymal Transition DOI Open Access
Ewa Błaszczak, Paulina Miziak, Adrian Odrzywolski

et al.

Cancers, Journal Year: 2025, Volume and Issue: 17(2), P. 228 - 228

Published: Jan. 12, 2025

Triple-negative breast cancer (TNBC) is one of the most difficult subtypes to treat due its distinct clinical and molecular characteristics. Patients with TNBC face a high recurrence rate, an increased risk metastasis, lower overall survival compared other subtypes. Despite advancements in targeted therapies, traditional chemotherapy (primarily using platinum compounds taxanes) continues be standard treatment for TNBC, often limited long-term efficacy. tumors are heterogeneous, displaying diverse mutation profile considerable chromosomal instability, which complicates therapeutic interventions. The development chemoresistance frequently associated process epithelial–mesenchymal transition (EMT), during epithelial tumor cells acquire mesenchymal-like phenotype. This shift enhances metastatic potential, while simultaneously reducing effectiveness chemotherapeutics. It has also been suggested that EMT plays central role stem cells. Hence, there growing interest exploring small-molecule inhibitors target as future strategy overcoming resistance improving outcomes patients TNBC. review focuses on progression drug emphasis these processes. We present TNBC-specific EMT-related features, key protein markers, various signaling pathways involved. discuss important mechanisms factors related within context EMT, highlighting improve patients’ outcomes.

Language: Английский

Citations

1

LAMB1 downregulation suppresses glioma progression by inhibiting aerobic glycolysis through regulation of the NF-κB/HK2 axis DOI Creative Commons
Zhenxiang Zhao, Haiying Liu, Yingzi Liu

et al.

Discover Oncology, Journal Year: 2025, Volume and Issue: 16(1)

Published: Feb. 7, 2025

Laminin subunit beta 1 (LAMB1) has regulatory functions on the proliferation, attachment, and migration of tumor cells, with increased levels linked to different cancers. This study aims at investigating effects mechanisms LAMB1 in glioma. Glioma cell models overexpression or downregulation were constructed. Cell viability, invasion evaluated. Glucose uptake lactate production examined, Seahorse was used assess extracellular acidification rate (ECAR). The EC50 temozolomide (TMZ) glioma cells tested. Western blotting conducted monitor expression HK1, HK2, PDHA, PKM. Bioinformatic analysis employed investigate downstream mechanism LAMB1. In addition, a subcutaneous model constructed determine influence GBM growth vivo. enhanced promoted growth. upregulation cellular glycolysis repressed sensitivity TMZ. activated NF-κB pathway. Downregulation mitigating pathway by Bay 11-7082 inhibited growth, TMZ sensitivity. exerted antitumor regulating NF-κB/HK2 axis.

Language: Английский

Citations

1

The role of the transcription factor NF-kB in the pathogenesis of inflammation and carcinogenesis. Modulation capabilities DOI Creative Commons

Maria Moneva-Sakelarieva,

Yozlem Kobakova,

Spiro Konstantinov

et al.

Pharmacia, Journal Year: 2025, Volume and Issue: 72, P. 1 - 13

Published: Feb. 20, 2025

The nuclear factor kappa B (NF-kB) signaling module is a complex and highly interconnected molecular network with important functions in all nucleated cells. Most chronic diseases caused by lifestyle factors appear to be related inflammation. NF-kB plays major role the pathogenesis of inflammation its intimate mechanism. This transcription participates evolution diabetes complications. In T1D (Type 1 Diabetes), proinflammatory cytokines such as interleukin-1β (IL-1β), tumor necrosis (TNF), CD40L secreted immune cells islets induce activation β-cells through both canonical noncanonical roads. increases expression genes, including TNF-α, IL-1β, IL-6, MCP-1, ICAM-1, that initiate promote atherosclerosis. particular, severity lethality acute lung injury or respiratory distress syndrome (ALI/ARDS) pneumonia sepsis primarily associated an NF-kB-mediated “cytokine storm,” which massive polymorphonuclear (PMN) extravasation subsequent release cause rapid deterioration due widespread coagulation. Nuclear translocation p65 can several genes involved induction EMT (epithelial-to-mesenchymal transition). has been confirmed various types cancer, brain, breast, lung, gastric cancer. Cutaneous T-cell lymphoma (CTCL) encompasses group lymphoproliferative disorders characterized invasive neoplastic T skin clinical prognoses. early stages CTCL, cell proliferation are stimulated autocrine production TNFα, leading increased resistance apoptosis. Bladder cancer second most common genitourinary often recurrent and/or chemoresistant after resection. critical normal physiology bladder patients have pathologically active induced cytokines, chemokines, hypoxia, enhancing carcinogenesis progression disease.

Language: Английский

Citations

1

Curcumin in the treatment of urological cancers: Therapeutic targets, challenges and prospects DOI
Mehrdad Hashemi, Sepideh Mirzaei,

Maryamsadat Barati

et al.

Life Sciences, Journal Year: 2022, Volume and Issue: 309, P. 120984 - 120984

Published: Sept. 20, 2022

Language: Английский

Citations

29

Long non-coding RNA/epithelial-mesenchymal transition axis in human cancers: Tumorigenesis, chemoresistance, and radioresistance DOI
Mehrdad Hashemi, Shima Hajimazdarany, Chakrabhavi Dhananjaya Mohan

et al.

Pharmacological Research, Journal Year: 2022, Volume and Issue: 186, P. 106535 - 106535

Published: Nov. 2, 2022

Language: Английский

Citations

29