Combined Poziotinib with Manidipine Treatment Suppresses Ovarian Cancer Stem-Cell Proliferation and Stemness

Lee, Heejin; Kim, Jun Woo; Lee, Dong‐Seok; Min, Sang‐Hyun

doi:10.3390/ijms21197379

Cited by 7 publications

(10 citation statements)

References 36 publications

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“…In addition, it triggered growth 1 (G1) cell cycle arrest and apoptosis. Furthermore, poziotinib decreased the stemming of CSCs and interfered with the pathways of Wnt/β-catenin, Notch, and Hedgehog that lead to CSC self-renewal [ 115 ]. Ovarian cancer stem cells have been scientifically shown to survive conventional chemotherapy [ 116 ].…”

Section: Her4 Inhibitorsmentioning

confidence: 99%

“…Although ovarian CSCs have not been clearly understood in this respect, a small population of chemo-resistant cancer cells may have the properties of cancer stem cells and play an important role in recurrence [ 117 , 118 ]. To interrupt cancer stem cell properties and stem cell signaling pathways, a novel approach is required [ 115 ].…”

Section: Her4 Inhibitorsmentioning

confidence: 99%

“…It was shown using Chou–Talalay method that combination therapy of poziotinib with manidipine (a dihydropyridine calcium antagonist) showed a synergistic effect in inhibiting ovarian CSCs more than in ovarian cancer cells as shown in Figure 3 [ 115 ]. Combination therapy with poziotinib and manidipine inhibited the expression of stem cell markers, especially CD133, NANOG, and KLF4.…”

Section: Her4 Inhibitorsmentioning

confidence: 99%

“…Combination therapy with poziotinib and manidipine inhibited the expression of stem cell markers, especially CD133, NANOG, and KLF4. The two drugs also inhibited the phosphorylation of STAT5, AKT, and ERK, which are involved in CSC self-renewal and β-catenin nuclear translocation [ 115 ].…”

Section: Her4 Inhibitorsmentioning

confidence: 99%

“…Poziotinib and manidipine combination therapy showed synergistic effect in inhibiting ovarian CSC by inhibiting HER4 and calcium channel mediated STAT5, AKT and ERK signaling [ 115 ].…”

Section: Her4 Inhibitorsmentioning

confidence: 99%

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A Review of HER4 (ErbB4) Kinase, Its Impact on Cancer, and Its Inhibitors

et al. 2021

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HER4 is a receptor tyrosine kinase that is required for the evolution of normal body systems such as cardiovascular, nervous, and endocrine systems, especially the mammary glands. It is activated through ligand binding and activates MAPKs and PI3K/AKT pathways. HER4 is commonly expressed in many human tissues, both adult and fetal. It is important to understand the role of HER4 in the treatment of many disorders. Many studies were also conducted on the role of HER4 in tumors and its tumor suppressor function. Mostly, overexpression of HER4 kinase results in cancer development. In the present article, we reviewed the structure, location, ligands, physiological functions of HER4, and its relationship to different cancer types. HER4 inhibitors reported mainly from 2016 to the present were reviewed as well.

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Section: Her4 Inhibitorsmentioning

confidence: 99%

Section: Her4 Inhibitorsmentioning

confidence: 99%

Section: Her4 Inhibitorsmentioning

confidence: 99%

Section: Her4 Inhibitorsmentioning

confidence: 99%

“…Poziotinib and manidipine combination therapy showed synergistic effect in inhibiting ovarian CSC by inhibiting HER4 and calcium channel mediated STAT5, AKT and ERK signaling [ 115 ].…”

Section: Her4 Inhibitorsmentioning

confidence: 99%

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A Review of HER4 (ErbB4) Kinase, Its Impact on Cancer, and Its Inhibitors

et al. 2021

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Causal relationship between thyroid dysfunction and ovarian cancer: a two-sample Mendelian randomization study

Wang,

et al. 2024

BMC Cancer

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Purpose Observational studies and clinical validation have suggested a link between thyroid dysfunction and an elevated ovarian cancer (OC) risk. However, whether this association indicates a cause-and-effect relationship remains uncertain. We aimed to investigate the plausible causal impact of thyroid dysfunction on OC through a Mendelian randomization (MR) study. Methods Genome-wide association study (GWAS) data for thyrotropin (TSH), free thyroxine (FT4), hypothyroidism, and hyperthyroidism were obtained as exposures and those for OC (N = 199,741) were selected as outcomes. Inverse variance-weighted method was used as the main estimation method. A series of sensitivity analyses, including Cochran’s Q test, MR-Egger intercept analysis, forest plot scatter plot, and leave-one-out test, was conducted to assess the robustness of the estimates. Results Genetic prediction of hyperthyroidism was associated with a potential increase in OC risk (odds ratio = 1.094, 95% confidence interval: 1.029–1.164, p = 0.004). However, no evidence of causal effects of hypothyroidism, TSH, and FT4 on OC or reverse causality was detected. Sensitivity analyses demonstrated consistent and reliable results, with no significant estimates of heterogeneity or pleiotropy. Conclusions This study employed MR to establish a correlation between hyperthyroidism and OC risk. By genetically predicting OC risk in patients with hyperthyroidism, our research suggests new insights for early prevention and intervention of OC.

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Targeting ovarian cancer stem cells: a new way out

Tian

Cui

2023

Stem Cell Res Ther

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Ovarian cancer (OC) is the most lethal gynecological malignancy due to tumor heterogeneity, the lack of reliable early diagnosis methods and the high incidence of chemoresistant recurrent disease. Although there are developments in chemotherapies and surgical techniques to improve the overall survival of OC patients, the 5-year survival of advanced OC patients is still low. To improve the prognosis of OC patients, it is important to search for novel therapeutic approaches. Cancer stem cells (CSCs) are a subpopulation of tumor cells that participate in tumor growth, metastasis and chemoresistance. It is important to study the role of CSCs in a highly heterogeneous disease such as OC, which may be significant to a better understanding of the oncogenetic and metastatic pathways of the disease and to develop novel strategies against its progression and platinum resistance. Here, we summarized the current findings about targeting methods against ovarian cancer stem cells, including related signaling pathways, markers and drugs, to better manage OC patients using CSC-based therapeutic strategies.

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Combined Poziotinib with Manidipine Treatment Suppresses Ovarian Cancer Stem-Cell Proliferation and Stemness

Cited by 7 publications

References 36 publications

A Review of HER4 (ErbB4) Kinase, Its Impact on Cancer, and Its Inhibitors

A Review of HER4 (ErbB4) Kinase, Its Impact on Cancer, and Its Inhibitors

Causal relationship between thyroid dysfunction and ovarian cancer: a two-sample Mendelian randomization study

Targeting ovarian cancer stem cells: a new way out

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