Increased ROS alters E-/N-cadherin levels and promotes migration in prostate cancer cells

Varisli, Lokman; Veysel, Veysel TOLAN

doi:10.4149/bll_2022_121

Cited by 4 publications

(3 citation statements)

References 29 publications

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“…In cancer, the activation of EMT switching mechanisms enables phenomena that are linked to de-differentiation and migration, which in combination with the reverse process from EMT, namely MET (mesenchymal to epithelial transition), facilitates metastasis [11][12][13][14][15][16]. What is important is that EMT-like phenomena confer a substantial degree of dynamic plasticity to cancer cell clones, which can function as cancer stem cells that have the properties of drug resistance and tumor initiation [17].…”

Section: Variations Of the Emt Theme In Cancermentioning

confidence: 99%

Epithelial–Mesenchymal Transition in Acute Leukemias

Varisli,

Vlahopoulos

2024

IJMS

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Epithelial–mesenchymal transition (EMT) is a metabolic process that confers phenotypic flexibility to cells and the ability to adapt to new functions. This transition is critical during embryogenesis and is required for the differentiation of many tissues and organs. EMT can also be induced in advanced-stage cancers, leading to further malignant behavior and chemotherapy resistance, resulting in an unfavorable prognosis for patients. Although EMT was long considered and studied only in solid tumors, it has been shown to be involved in the pathogenesis of hematological malignancies, including acute leukemias. Indeed, there is increasing evidence that EMT promotes the progression of acute leukemias, leading to the emergence of a more aggressive phenotype of the disease, and also causes chemotherapy resistance. The current literature suggests that the levels and activities of EMT inducers and markers can be used to predict prognosis, and that targeting EMT in addition to conventional therapies may increase treatment success in acute leukemias.

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Section: Variations Of the Emt Theme In Cancermentioning

confidence: 99%

Epithelial–Mesenchymal Transition in Acute Leukemias

Varisli,

Vlahopoulos

2024

IJMS

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“…Neuro(N)-cadherin is a single-chain transmembrane glycoprotein that is dependent on calcium and mediates homotypic and heterotypic cell-cell adhesion [33]. The reduced expression of N-cadherin leads to an impact on prostate cancer cell invasion, migration and epithelial-to-mesenchymal transition [34,35]. In our experiment, the two-drug combination group increased the expression of E-cadherin protein (Figure 6E) and decreased the expression of N-cadherin protein in the tumor tissues of the aforementioned groups (Figure 6F) compared with the control group.…”

Section: Kaempferol Combined With Docetaxel Inhibits Prostate Cancer ...mentioning

confidence: 99%

Combination of Kaempferol and Docetaxel Induces Autophagy in Prostate Cancer Cells In Vitro and In Vivo

Zhou,

Fang,

Pang

et al. 2023

IJMS

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Docetaxel is a first-line chemotherapy drug used to treat advanced prostate cancer, but patients who have used it often face the challenges of drug resistance and side effects. Kaempferol is a naturally occurring flavonol; our previous studies have confirmed that it has excellent anti-prostate activity. To investigate the anti-prostate cancer effects of docetaxel in combination with kaempferol, we conducted experiments at the cellular and whole-animal level. Plate cloning assays showed that the combination of docetaxel and kaempferol had a synergistic effect in inhibiting the proliferation of prostate cancer cells. The combination of these two compounds was found to induce autophagy in prostate cancer cells via transmission electron microscopy, and changes in the expression of autophagy-related proteins via Western blot assays also confirmed the occurrence of autophagy at the molecular level. We also confirmed the anti-prostate cancer effect of docetaxel in combination with kaempferol in vivo by establishing a mouse xenograft prostate cancer model. Autophagy-related proteins were also examined in mouse tumor tissues and verified the presence of autophagy in mouse tumor tissues. The above cellular and animal data suggest that docetaxel in combination with kaempferol has significant anti-prostate cancer effects and that it works by inducing autophagy in cells.

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“…E-cadherin loss is observed in the advanced stages of many cancers, including BCa, and this event is a strong marker of EMT [212]. Cadherin switching in advanced stages of cancers is generally associated with an increase in the invasive and metastatic potential of cancer cells, and this event may be the result of various mechanisms that are triggered by genetic or epigenetic alterations [212,213]. Furthermore, it may also be a result of therapeutic approaches, such as androgen deprivation therapy in prostate cancer [214].…”

Section: Src-3 Promotes Malignant Behaviors Of Tumor Cellsmentioning

confidence: 99%

Critical Roles of SRC-3 in the Development and Progression of Breast Cancer, Rendering It a Prospective Clinical Target

Varisli,

Dancik,

Tolan

et al. 2023

Cancers

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Breast cancer (BCa) is the most frequently diagnosed malignant tumor in women and is also one of the leading causes of cancer-related death. Most breast tumors are hormone-dependent and estrogen signaling plays a critical role in promoting the survival and malignant behaviors of these cells. Estrogen signaling involves ligand-activated cytoplasmic estrogen receptors that translocate to the nucleus with various co-regulators, such as steroid receptor co-activator (SRC) family members, and bind to the promoters of target genes and regulate their expression. SRC-3 is a member of this family that interacts with, and enhances, the transcriptional activity of the ligand activated estrogen receptor. Although SRC-3 has important roles in normal homeostasis and developmental processes, it has been shown to be amplified and overexpressed in breast cancer and to promote malignancy. The malignancy-promoting potential of SRC-3 is diverse and involves both promoting malignant behavior of tumor cells and creating a tumor microenvironment that has an immunosuppressive phenotype. SRC-3 also inhibits the recruitment of tumor-infiltrating lymphocytes with effector function and promotes stemness. Furthermore, SRC-3 is also involved in the development of resistance to hormone therapy and immunotherapy during breast cancer treatment. The versatility of SRC-3 in promoting breast cancer malignancy in this way makes it a good target, and methodical targeting of SRC-3 probably will be important for the success of breast cancer treatment.

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Increased ROS alters E-/N-cadherin levels and promotes migration in prostate cancer cells

Cited by 4 publications

References 29 publications

Epithelial–Mesenchymal Transition in Acute Leukemias

Epithelial–Mesenchymal Transition in Acute Leukemias

Combination of Kaempferol and Docetaxel Induces Autophagy in Prostate Cancer Cells In Vitro and In Vivo

Critical Roles of SRC-3 in the Development and Progression of Breast Cancer, Rendering It a Prospective Clinical Target

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