Expression of matrix metalloproteinase-10 in non-metastatic prostate cancer: Correlation with an imbalance in cell proliferation and apoptosis

Maruta, Sugure; Miyata, Yasuyoshi; Sagara, Yuji; Kanda, Shigeru; Iwata, Tohru; Watanabe, Soichi; Sakai, Hideki; Hayashi, Tomayoshi; Kanetake, Hiroshi

doi:10.3892/ol_00000073

Cited by 11 publications

(12 citation statements)

References 20 publications

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“…In particular, compared to other MMPs, MMP-10 has a relatively broad substrate specificity and has been demonstrated to degrade a variety of matrix and non-matrix components (Bodey et al, 2001). Besides mainly participating in tumor invasion and metastasis, MMP-10 were even found to inhibit cancer cell apoptosis (Maruta et al, 2010). Therefore, proapoptotic activity of chrysin may also correlate with the inhibition of MMP-10.…”

Section: Discussionmentioning

confidence: 99%

Chrysin inhibits metastatic potential of human triple‐negative breast cancer cells by modulating matrix metalloproteinase‐10, epithelial to mesenchymal transition, and PI3K/Akt signaling pathway

Yang

Huang

Xiang

et al. 2013

J of Applied Toxicology

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Chrysin, a naturally occurring flavone, has been shown to inhibit cell proliferation and induce cell apoptosis in various cancers. However, the effect and mechanisms of chrysin on cancer metastasis are still enigmatic. In this study, metastatic triple-negative breast cancer (TNBC) cell lines were used to evaluate the antimetastatic activity of chrysin. The results showed that chrysin (5, 10 and 20 μM) significantly suppressed TNBC cell migration and invasion in a dose-dependent manner. Human matrix metalloproteinase (MMP) antibody array demonstrated that MMP-10 was downregulated by chrysin, which was further verified by Western blotting and ELISA. Moreover, it was shown that chrysin induced increased E-cadherin expression and decreased expression of vimentin, snail and slug in TNBC cells, suggesting that chrysin had a reversal effect on epithelial-mesenchymal transition. More importantly, it was demonstrated that inhibiting the Akt signal pathway might play a central role in chrysin-induced antimetastatic activity by regulating MMP-10 and epithelial-mesenchymal transition. In conclusion, our study indicates that chrysin exerts antimetastatic activities in TNBC cells, which suggests that chrysin might be a potential therapeutic candidate for the treatment of advanced or metastatic breast cancer.

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Section: Discussionmentioning

confidence: 99%

Chrysin inhibits metastatic potential of human triple‐negative breast cancer cells by modulating matrix metalloproteinase‐10, epithelial to mesenchymal transition, and PI3K/Akt signaling pathway

Yang

Huang

Xiang

et al. 2013

J of Applied Toxicology

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“…Additionally, they speculated that MMP-10 modulates tumor growth via the regulation of the balance of cell proliferation and apoptosis. 88 Singh et al showed that interactions between chemokine receptor CXCR5 and chemokine CXCL13 had an influence to the expression of MPP-10 in PCa. In cell lines of PCa cultured with or without CXCL13, changes in expression of MMP-10 was observed.…”

Section: Mmp-10 In Carcinogenesis Of Cancersmentioning

confidence: 99%

<p>Matrilysins and Stromelysins in Pathogenesis and Diagnostics of Cancers</p>

Piskór¹,

Przylipiak²,

Dąbrowska³

et al. 2020

CMAR

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Matrix metalloproteinases (MMPs) are endopeptidases which are widely studied in terms of their role in the physiological and pathological processes in the organism. In this article, we consider usefulness of matrilysins and stromelysins in pathogenesis and diagnostic of the most common malignancies in the world, e.g., lung, breast, prostate, and colorectal cancers. In all of the mentioned cancers, matrilysins and stromelysins have a pivotal role in their development and also may have diagnostic utility. Influence to the cancerous process is connected with specific dependencies between these enzymes and components of the extracellular matrix (ECM), non-matrix components like cell surface components. All the information provided below allows to take a closer look at matrilysins and stromelysins and their functions in the cancer development.

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“…2F), indicating a role for LIMK activity in androgen-induced motility. Expression of the matrix metalloproteinases MMP-10 (35) and MMP-1 (36), which had previously been implicated in prostate tumor growth, were not affected by DHT or LIMKi treatment (Supplementary Fig S1D). Interestingly, when LNCaP cells were treated with 10 μM LIMKi we readily observed reduced LNCaP cell numbers.…”

Section: Resultsmentioning

confidence: 84%

Elevated LIM Kinase 1 in Nonmetastatic Prostate Cancer Reflects Its Role in Facilitating Androgen Receptor Nuclear Translocation

Mardilovich

Gabrielsen

McGarry

et al. 2015

Molecular Cancer Therapeutics

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Prostate cancer affects a large proportion of the male population, and is primarily driven by androgen receptor (AR) activity. First-line treatment typically consists of reducing AR signaling by hormone depletion, but resistance inevitably develops over time. One way to overcome this issue is to block AR function via alternative means, preferably by inhibiting protein targets that are more active in tumors than in normal tissue. By staining prostate cancer tumor sections, elevated LIM kinase 1 (LIMK1) expression and increased phosphorylation of its substrate Cofilin were found to be associated with poor outcome and reduced survival in patients with nonmetastatic prostate cancer. A LIMKselective small molecule inhibitor (LIMKi) was used to determine whether targeted LIMK inhibition was a potential prostate cancer therapy. LIMKi reduced prostate cancer cell motility, as well as inhibiting proliferation and increasing apoptosis in androgendependent prostate cancer cells more effectively than in androgenindependent prostate cancer cells. LIMK inhibition blocked ligand-induced AR nuclear translocation, reduced AR protein stability and transcriptional activity, consistent with its effects on proliferation and survival acting via inhibition of AR activity. Furthermore, inhibition of LIMK activity increased aTubulin acetylation and decreased AR interactions with aTubulin, indicating that the role of LIMK in regulating microtubule dynamics contributes to AR function. These results indicate that LIMK inhibitors could be beneficial for the treatment of prostate cancer both by reducing nuclear AR translocation, leading to reduced proliferation and survival, and by inhibiting prostate cancer cell dissemination.

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Expression of matrix metalloproteinase-10 in non-metastatic prostate cancer: Correlation with an imbalance in cell proliferation and apoptosis

Cited by 11 publications

References 20 publications

Chrysin inhibits metastatic potential of human triple‐negative breast cancer cells by modulating matrix metalloproteinase‐10, epithelial to mesenchymal transition, and PI3K/Akt signaling pathway

Chrysin inhibits metastatic potential of human triple‐negative breast cancer cells by modulating matrix metalloproteinase‐10, epithelial to mesenchymal transition, and PI3K/Akt signaling pathway

<p>Matrilysins and Stromelysins in Pathogenesis and Diagnostics of Cancers</p>

Elevated LIM Kinase 1 in Nonmetastatic Prostate Cancer Reflects Its Role in Facilitating Androgen Receptor Nuclear Translocation

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