Suppression of PMA-induced tumor cell invasion by capillarisin via the inhibition of NF-κB-dependent MMP-9 expression

Lee, Syng‐Ook; Jeong, Yun-Jeong; Kim, Mi‐Hyun; Kim, Cheorl-Ho; Lee, In-Seon

doi:10.1016/j.bbrc.2007.12.068

Cited by 71 publications

(70 citation statements)

References 22 publications

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“…Huang et al demonstrates that stromal cell-derived factor-1/CXCR4 enhances the motility of human osteosarcoma cells that involve MEK1/2, ERK and NF-κB-dependent pathways (Huang et al, 2009); in addition, CXCR4 mediates the homing of B cell progenitor acute lymphoblastic leukaemia cells to the bone marrow via the activation of p38MAPK (Juarez et al, 2009). Moreover, the reduction of ERK1/2 signaling pathways resulted in the inhibition of MMP-9 expression in arterialized vein grafts (Sharony et al, 2006), a p38 MAPK inhibitor (SB203580) suppresses the regulation of MMP-9 in cancer cells (Simon et al, 1998), and the suppression of the JNK pathway leads to a downregulated PMA-induced MMP-9 expression (Lee et al, 2008). Thus, in our study, the inhibitory effects of nobiletin on the expressions of CXCR4 and MMP-9 may be mediated in part through the inactivation of the MAPKs pathways.…”

Section: Discussionmentioning

confidence: 99%

Antimetastatic effect of nobiletin through the down-regulation of CXC chemokine receptor type 4 and matrix metallopeptidase-9

Baek

Kim

Nam

et al. 2012

Pharmaceutical Biology

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Section: Discussionmentioning

confidence: 99%

Antimetastatic effect of nobiletin through the down-regulation of CXC chemokine receptor type 4 and matrix metallopeptidase-9

Baek

Kim

Nam

et al. 2012

Pharmaceutical Biology

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“…Tumor metastasis is a multistep process by which a subset of individual cancer cells disseminates from a primary tumor to distant secondary organs or tissues. This process involves cell proliferation, ECM degradation, cell migration, and tumor growth at metastatic sites (13,15). Tumor cell invasion is an early step in the metastatic cascade, representing the beginning of the transition from the benign stage to malignancy.…”

Section: Discussionmentioning

confidence: 99%

“…MMP-9 is reported to be a key enzyme for degrading type IV collagen, which is a major component of the basement membrane. Elevated MMP-9 levels are functionally linked to elevated metastasis in a number of tumors, including those of the brain (9), prostate (10), bladder (11) and breast (12,13). Several mechanisms regulate MMP-9 activity, including gene transcription, proenzyme activation, and endogenous inhibitors such as tissue inhibitors of metalloproteinases (TIMPs).…”

Section: Introductionmentioning

confidence: 99%

“…A variety of stimuli, including cytokines and phorbol ester, stimulate MMP-9 synthesis and secretion during various pathological processes such as tumor invasion, atherosclerosis, inflammation, and rheumatoid arthritis. MMP-2, on the other hand, is usually expressed constitutively (13,14). Cytokine and 12-O-tetradecanoyl phorbol-13-acetate (TPA) treatments are capable of inducing MMP-9 expression via the activation of transcription factors such as NF-κB and activator protein-1 (AP-1) (15)(16)(17).…”

Section: Introductionmentioning

confidence: 99%

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Radix clematidis extract inhibits TPA-induced MMP-9 expression by suppressing NF-κB activation in MCF-7 human breast cancer cells

et al. 2011

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Abstract. Matrix metalloproteinase-9 (MMP-9), which degrades the extracellular matrix (ECM), plays an important role in breast cancer pathogenesis. Previously, we reported that the Radix clematidis extract (RCE) inhibits MMP expression by suppressing the nuclear factor-κB (NF-κB) pathway. The purpose of the present study was to investigate the effects of RCE on 12-O-tetradecanoyl phorbol-13-acetate (TPA)-induced MMP-9 expression and cell invasion in MCF-7 cells. The toxicity of RCE was determined by MTT assay. MMP-9 expression was determined by real-time PCR, zymography and Western blot analysis. NF-κB activation was assayed by electrophoretic mobility shift assay (EMSA). Results showed that the expression of MMP-9 and cell invasion in response to TPA was increased, whereas TPA-induced MMP-9 expression and cell invasion was decreased by RCE. Moreover, RCE suppressed NF-κB activation in TPA-treated MCF-7 cells. Thus, RCE is a potent inhibitor of TPA-induced MMP-9 expression and markedly blocks the NF-κB pathway in MCF-7 cells.

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“…12-O-tetradecanoylphorbol-13-acetate (TPA) is a tumor promoter and promotes invasion of breast cancer cells (MCF-7) by inducing MMP-9 via protein kinase C (PKC) pathways (14,41). In fact, TPA activates PKCs by binding to the Cl domain.…”

Section: Curcumin Suppresses the Expression Of Matrix Metalloproteinamentioning

confidence: 99%

Molecular Mechanisms of Anti-metastatic Activity of Curcumin

Deng

Verron

Rohanizadeh

2016

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Abstract. Cancer is the leading cause of death worldwide. Although cancer occurs as a localized disease, its morbidity and mortality rates remain high due to the ability of cancer cells to break-off from the primary tumor and spread to distant organs. Currently, chemotherapy is the main treatment for cancer; however, the increase in proportion of drug-resistant cancer cells and unpleasant side-effects of chemotherapy are still the major challenges in cancer therapy. Curcumin is a natural polyphenol compound and the main bioactive constituent of Indian spice turmeric, widely used in Indian and Chinese medicines. Curcumin has well-known therapeutic actions, including antiinflammatory, anti-microbial, anti-oxidant and anti-cancer properties. Curcumin induces cancer cell apoptosis through regulating various signaling pathways and arresting tumor cell cycle. Curcumin's therapeutic/ preventative actions on metastatic cancers have not been yet fully understood and studied. The present review explores the potential anti-metastatic mechanisms of curcumin, including inhibition of transcription factors and their signaling pathways (e.g., inflammatory cytokines (e.g., CXCL1, CXCL2, multiple proteases (e.g., uPA, MMPs), multiple protein kinases (e.g., MAPKs, FAK), regulation of miRNAs (e.g., miR21, miR181b) and heat shock proteins (HLJ1). In addition, possible synergistic actions of combination therapy of curcumin with current chemotherapies are discussed in this review.Despite all recent advances in oncology, cancer is still one of the deadliest diseases around the world (1). Cancer occurs as a localized disease but can spread to distant organs through migration, invasion and metastasis (2). Metastatic cancer is one of the major causes of death in cancer patients. Metastasis is a complex process involving multiple steps: (i) local migration through degrading basement membrane and extracellular matrix (ECM), (ii) intravasation into blood and/or lymphatic vessels, (iii) circulating to the target organ site, (iv) extravasation into target organ tissue and, finally, (v) multiplication in the target organ (2, 3). These steps are mediated by various factors, including growth factors, proteolysis degradation of extracellular matrix, cell-cell adhesion, cytoskeleton remodeling and changes of genes' expressions (2, 3). Metastasis is a non-random process that means each metastatic cancer type has its own preferred site of metastasis. For example, breast cancer cells preferentially metastasize to regional lymph nodes, liver, lungs and bone (4). Nowadays, there are different therapeutic approaches available for patients with metastatic cancers, including surgery, radiotherapy and chemotherapy. Chemotherapy remains the main treatment modality for cancer patients because of its ability of preventing invasion and metastasis. However, the morbidity and mortality rates in patients with metastatic cancer still remain high since current chemotherapy agents fail to selectively and effectively kill cancer cells without destroying normal ce...

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Suppression of PMA-induced tumor cell invasion by capillarisin via the inhibition of NF-κB-dependent MMP-9 expression

Cited by 71 publications

References 22 publications

Antimetastatic effect of nobiletin through the down-regulation of CXC chemokine receptor type 4 and matrix metallopeptidase-9

Antimetastatic effect of nobiletin through the down-regulation of CXC chemokine receptor type 4 and matrix metallopeptidase-9

Radix clematidis extract inhibits TPA-induced MMP-9 expression by suppressing NF-κB activation in MCF-7 human breast cancer cells

Molecular Mechanisms of Anti-metastatic Activity of Curcumin

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