Innovating Cancer Treatment Through Cell Cycle, Telomerase, Angiogenesis, and Metastasis DOI
Tooba Yousefi, Bahareh Mohammadi Jobani,

Reyhaneh Taebi

и другие.

DNA and Cell Biology, Год журнала: 2024, Номер unknown

Опубликована: Июль 17, 2024

Cancer remains a formidable challenge in the field of medicine, necessitating innovative therapeutic strategies to combat its relentless progression. The cell cycle, tightly regulated process governing growth and division, plays pivotal role cancer development. Dysregulation cycle allows cells proliferate uncontrollably. Therapeutic interventions designed disrupt offer promise restraining tumor Telomerase, an enzyme responsible for maintaining telomere length, is often overactive cells, conferring them with immortality. Targeting telomerase presents opportunity limit replicative potential hinder growth. Angiogenesis, formation new blood vessels, essential metastasis. Strategies aimed at inhibiting angiogenesis seek deprive tumors their vital supply, thereby impeding Metastasis, spread from primary distant sites, major therapy. Research efforts are focused on understanding underlying mechanisms metastasis developing this deadly process. This review provides glimpse into multifaceted approach therapy, addressing critical aspects biology-cell regulation, activity, angiogenesis, Through ongoing research strategies, oncology continues advance, offering hope improved treatment outcomes enhanced quality life patients.

Язык: Английский

KMT2D‐mediated H3K4me1 recruits YBX1 to facilitate triple‐negative breast cancer progression through epigenetic activation of c‐Myc DOI Creative Commons
Bing Yao, Mengying Xing, Xiangwei Zeng

и другие.

Clinical and Translational Medicine, Год журнала: 2024, Номер 14(7)

Опубликована: Июль 1, 2024

Abstract Background Lysine methyltransferase 2D (KMT2D) mediates mono‐methylation of histone H3 lysine 4 (H3K4me1) in mammals. H3K4me1 mark is involved establishing an active chromatin structure to promote gene transcription. However, the precise molecular mechanism underlying KMT2D‐mediated modulates expression triple‐negative breast cancer (TNBC) progression unresolved. Methods and Results We recognized Y‐box‐binding protein 1 (YBX1) as a “reader” mark, point mutation YBX1 (E121A) disrupted this interaction. found that KMT2D cooperatively promoted cell growth metastasis TNBC cells vitro vivo. The levels were both upregulated tumour tissues correlated with poor prognosis for patients. Combined analyses ChIP‐seq RNA‐seq data indicated was co‐localized promoter regions c‐Myc SENP1, thereby activating their expressions cells. Moreover, we demonstrated activated SENP1 KMT2D‐dependent manner. Conclusion Our results suggest recruits facilitate through epigenetic activation SENP1. These together unveil crucial interplay between regulation progression, thus providing novel insights into targeting KMT2D‐H3K4me1‐YBX1 axis treatment. Highlights H3K4me1‐binding effector disrupts its binding H3K4me1. proliferation by colocalized increased predicts

Язык: Английский

Процитировано

4
SOD1 inhibition enhances sorafenib efficacy in HBV‐related hepatocellular carcinoma by modulating PI3K/Akt/mTOR pathway and ROS‐mediated cell death DOI Creative Commons
Jooyoung Lee, Ji-Ye Kim,

Ryunjin Lee

и другие.

Journal of Cellular and Molecular Medicine, Год журнала: 2024, Номер 28(14)

Опубликована: Июль 1, 2024

Abstract Hepatitis B Virus (HBV) infection significantly elevates the risk of hepatocellular carcinoma (HCC), with HBV X protein (HBx) playing a crucial role in cancer progression. Sorafenib, primary therapy for advanced HCC, shows limited effectiveness HBV‐infected patients due to HBx‐related resistance. Numerous studies have explored combination therapies overcome this Sodium diethyldithiocarbamate (DDC), known its anticancer effects and inhibition superoxide dismutase 1 (SOD1), is hypothesized counteract sorafenib (SF) resistance HBV‐positive HCCs. Our research demonstrates that combining DDC SF reduces HBx SOD1 expressions HCC cells human tissues. This disrupts PI3K/Akt/mTOR signalling pathway promotes apoptosis by increasing reactive oxygen species (ROS) levels. These cellular changes lead reduced tumour viability enhanced sensitivity SF, as evidenced synergistic suppression growth xenograft models. Additionally, DDC‐mediated further enhances xenografted animals, thereby inhibiting progression more effectively. findings suggest DDC‐SF could serve promising strategy overcoming HBV‐related potentially optimizing outcomes.

Язык: Английский

Процитировано

4
Quercetin and taxifolin inhibits TMPRSS2 activity and its interaction with EGFR in paclitaxel‐resistant breast cancer cells: An in silico and in vitro study DOI Open Access

Durga Bhavani Kundrapu,

Krishna Chaitanya Amajala,

Kothapalli Manaswi

и другие.

Chemical Biology & Drug Design, Год журнала: 2024, Номер 104(2)

Опубликована: Июль 29, 2024

Abstract Transmembrane protease/serine (TMPRSS2), a type II transmembrane serine protease, plays crucial role in different stages of cancer. Recent studies have reported that the triggering epidermal growth factor receptor (EGFR) activation through protease action promotes metastasis. However, there are no reports on interaction TMPRSS2 with EGFR, especially triple‐negative triple negative (TNBC). The current study investigates unexplored between and which key partners mediating This is explored for potential targeting using quercetin (QUE) taxifolin (TAX). expression patterns breast cancer (BC) tissues subtypes been predicted, prognostic significance assessed GENT2.0 database. Validation was performed normal TNBC tissues, including drug‐resistant cell lines, utilizing GEO datasets. further validated as predictive biomarker FDA‐approved chemotherapeutics transcriptomic data from BC patients. demonstrated association EGFR silico analysis validates findings cohorts TIMER2.0 web server TCGA dataset C‐Bioportal. Molecular docking molecular dynamic simulation identified QUE TAX best leads TMPRSS2. They inhibited cell‐free activity like clinical inhibitor TMPRSS2, Camostat mesylate. In cell‐based assays focused paclitaxel‐resistant (TNBC/PR), potent inhibitory against extracellular membrane‐bound low IC 50 values. Furthermore, ELISA AlphaLISA inhibit EGFR. Additionally, exhibited significant inhibition proliferation cycle accompanied by notable alterations morphology TNBC/PR cells. provides valuable insights into overexpressing TNBC.

Язык: Английский

Процитировано

4
Fibroblast Growth Factor Receptor 4 Promotes Triple‐Negative Breast Cancer Progression via Regulating Fatty Acid Metabolism Through the AKT/RYR2 Signaling DOI Creative Commons

Jinhui Ye,

Song Wu,

Qiang Quan

и другие.

Cancer Medicine, Год журнала: 2024, Номер 13(23)

Опубликована: Дек. 1, 2024

Triple-negative breast cancer (TNBC) is the most aggressive subtype of cancer. Previous studies have found that fibroblast growth factor receptor 4 (FGFR4) plays a crucial role in tumor development and metastasis. However, potential underlying mechanisms FGFR4 progression TNBC remain unclear.

Язык: Английский

Процитировано

4
Innovating Cancer Treatment Through Cell Cycle, Telomerase, Angiogenesis, and Metastasis DOI
Tooba Yousefi, Bahareh Mohammadi Jobani,

Reyhaneh Taebi

и другие.

DNA and Cell Biology, Год журнала: 2024, Номер unknown

Опубликована: Июль 17, 2024

Cancer remains a formidable challenge in the field of medicine, necessitating innovative therapeutic strategies to combat its relentless progression. The cell cycle, tightly regulated process governing growth and division, plays pivotal role cancer development. Dysregulation cycle allows cells proliferate uncontrollably. Therapeutic interventions designed disrupt offer promise restraining tumor Telomerase, an enzyme responsible for maintaining telomere length, is often overactive cells, conferring them with immortality. Targeting telomerase presents opportunity limit replicative potential hinder growth. Angiogenesis, formation new blood vessels, essential metastasis. Strategies aimed at inhibiting angiogenesis seek deprive tumors their vital supply, thereby impeding Metastasis, spread from primary distant sites, major therapy. Research efforts are focused on understanding underlying mechanisms metastasis developing this deadly process. This review provides glimpse into multifaceted approach therapy, addressing critical aspects biology-cell regulation, activity, angiogenesis, Through ongoing research strategies, oncology continues advance, offering hope improved treatment outcomes enhanced quality life patients.

Язык: Английский

Процитировано

3