pSTAT3 expression associated with survival and mammographic density of breast cancer patients

Radenković, Sandra; Konjević, Gordana; Gavrilović, D.; Stojanović-Rundić, Suzana; Plesinac-Karapandzic, Vesna; Stevanović, Predrag; Jurišić, Vladimir

doi:10.1016/j.prp.2018.12.023

Cited by 14 publications

(12 citation statements)

References 26 publications

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“…Antibodies against the β subunit of ATPase show angiostatin-like properties and are cytotoxic to tumor cells by regulating intracellular pH [14]. Many of the examined markers were of greater or lesser clinical significance [15][16][17][18].…”

Section: Introductionmentioning

confidence: 99%

The function of Cav-1 in MDA-MB-231 breast cancer cell migration and invasion induced by ectopic ATP5B

Dong

et al. 2021

Med Oncol

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Ectopic ATP5B, which is located in a unique type of lipid raft caveolar structure, can be upregulated by cholesterol loading. As the structural component of caveolae, Cav-1 is a molecular hub that is involved in transmembrane signaling. In a previous study, the ATP5B-specific binding peptide B04 was shown to inhibit the migration and invasion of prostate cancer cells, and the expression of ATP5B on the plasma membrane of MDA-MB-231 cells was confirmed. The present study investigated the effect of ectopic ATP5B on the migration and invasion of MDA-MB-231 cells and examined the involvement of Cav-1. Cholesterol loading increased the level of ectopic ATP5B and promoted cell migration and invasion. These effects were blocked by B04. Ectopic ATP5B was physically colocalized with Cav-1, as demonstrated by double immunofluorescence staining and coimmunoprecipitation. After Cav-1 knockdown, the migration and invasion abilities of MDA-MB-231 cells were significantly decreased, suggesting that Cav-1 influences the function of ectopic ATP5B. Furthermore, these effects were not reversed after treatment with cholesterol. We concluded that Cav-1 may participate in MDA-MB-231 cell migration and invasion induced by binding to ectopic ATP5B.

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Section: Introductionmentioning

confidence: 99%

The function of Cav-1 in MDA-MB-231 breast cancer cell migration and invasion induced by ectopic ATP5B

Dong

et al. 2021

Med Oncol

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“…AP‐1 factors, along with other factors (NF‐ κ B, STATs (signal transducers and activators of transcription)) affect breast cancer cells proliferation. It was found that phosphorylated STAT3 expression is associated with survival and mammographic density of breast cancer patients . Moreover, various natural compounds, including 3‐deoxy‐2 β ,16‐dihydroxynagilactone E, apigenin, genistein, inhibit STAT3 signaling and induce apoptosis in cancer cells .…”

Section: Resultsmentioning

confidence: 99%

“…It was found that phosphorylated STAT3 expression is associated with survival and mammographic density of breast cancer patients. [37] Moreover, various natural compounds, including 3-deoxy-2β,16-dihydroxynagilactone E, apigenin, genistein, inhibit STAT3 signaling and induce apoptosis in cancer cells. [38 -41] Therefore, proteins in pathways that are altered during the Chem.…”

Section: Erα-related Pathwaysmentioning

confidence: 99%

Biological Evaluation of a New Brassinosteroid: Antiproliferative Effects and Targeting Estrogen Receptor α Pathways

Scherbakov

Жабинский

Хрипач

et al. 2019

Chemistry & Biodiversity

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Brassinosteroids (BS), a class of plant‐specific steroid hormones, are considered as new potential anticancer agents for the treatment of tumors of different origin, including hormone‐dependent cancers. Effects of a synthetic brassinosteroid BS4 ((22R,23R,24R)‐22,23‐dihydroxy‐24‐methyl‐B‐homo‐7‐oxa‐5α‐cholest‐2‐en‐6‐one ((3aS,7aR,7bS,9aS,10R,12aS,12bS)‐10‐[(2S,3R,4R,5R)‐3,4‐dihydroxy‐5,6‐dimethylheptan‐2‐yl]‐7a,9a‐dimethyl‐1,3a,4,7,7a,7b,8,9,9a,10,11,12,12a,12b‐tetradecahydro‐3H‐benzo[c]indeno[5,4‐e]oxepin‐3‐one)) on hormone‐dependent breast cancer cells and normal epithelial cells and its impact on the estrogen receptor signaling were evaluated. Cytotoxicity was assessed by MTT‐test; expression of estrogen receptor α and survivin was measured by immunoblotting. Transactivation analysis of luciferase reporter gene was performed for ERα and AP‐1 factors after the brassinosteroid treatment. Dock6 and Autodock Vina were used for molecular docking. BS4 revealed a significant antiproliferative effect towards the hormone‐dependent breast cancer cells and was not active against normal epithelial cells. BS4 action on MCF‐7 breast cancer cells was found to be complex: a decrease in ERα expression as well as in its transcription activity was accompanied by inhibition of ERα‐related signaling pathways (AP‐1 complex and survivin). BS4 binding mode to ERα ligand‐binding domain was analyzed by molecular docking. The obtained results show that antiproliferative and antiestrogenic properties of the brassinosteroid BS4, as well as its ability to inhibit the anti‐apoptotic protein survivin may be of interest for further development of anticancer agents.

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“…Recent studies have pointed out that deregulation of the Janus kinase (JAK) and signal transducer and activator of transcription (STAT) signaling pathway might be implicated in the pathogenesis of a variety of inflammatory diseases, autoimmune diseases, and malignancies. [2][3][4][5][6][7] Aberrant activation of STAT3 and STAT5 has already been demonstrated in malignant cell lines and blood derived from CTCL. [8][9][10][11][12][13][14][15] However, data concerning STAT expression in skin are rather scarce.…”

Section: Introductionmentioning

confidence: 98%

Mapping signal transducer and activator of transcription (STAT) activity in different stages of mycosis fungoides and Sezary syndrome

et al. 2020

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Background Deregulation of signal transducer and activator of transcription (STAT) signaling is known to participate in the pathogenesis of cutaneous T‐cell lymphomas (CTCLs). However, published results regarding STAT expression in different stages of CTCLs are conflicting. The aim of the study was to define the pattern of STAT expression in skin and detect any differences between pruritic and nonpruritic patients but also different stages of disease. Methods Thirty‐nine skin biopsies from CTCL patients and 24 biopsies from healthy volunteers were taken. Immunohistochemical staining for STAT 3, 5a, 5b, and 6 was performed in formalin‐fixed paraffin‐embedded sections of mycosis fungoides (MF) and Sezary syndrome (SS) specimens. Results We found increased expression of STAT proteins in CTCL: MF and SS skin in comparison to the control group. STAT5 but also STAT6 and to a lesser extent STAT3 seems to be constitutively activated in MF and SS. Moreover, also downregulation of STAT5b protein in advanced‐stage CTCL appears to contribute to its pathogenesis. There were no significant associations between expression of STATs and pruritus severity. Conclusions Our results confirm the possible pathogenetic role of STATs in CTCL. STATs seem to be a promising target for new effective therapeutic agents in CTCL.

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pSTAT3 expression associated with survival and mammographic density of breast cancer patients

Cited by 14 publications

References 26 publications

The function of Cav-1 in MDA-MB-231 breast cancer cell migration and invasion induced by ectopic ATP5B

The function of Cav-1 in MDA-MB-231 breast cancer cell migration and invasion induced by ectopic ATP5B

Biological Evaluation of a New Brassinosteroid: Antiproliferative Effects and Targeting Estrogen Receptor α Pathways

Mapping signal transducer and activator of transcription (STAT) activity in different stages of mycosis fungoides and Sezary syndrome

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