The role of matrix metalloproteinases in cancer progression, in particular metastasis

Alsayad, Fatima A. S.

doi:10.5114/amscd.2018.81070

Cited by 3 publications

(3 citation statements)

References 245 publications

(342 reference statements)

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“…[24][25][26] It is reported that rate of metastasis of tumor cells is directly related with the expression of MMPs in the cells. 24,27,28 In the current study, tretinoin treatment led to a prominent reduction in MMP-2 and MMP-9 expression in HT-3 cervical cancer cells in dose-dependent manner. Increase in concentration of tretinoin caused more prominent decease in expression of MMP-2 and MMP-9 proteins in HT-3 cells.…”

Section: Discussionsupporting

confidence: 55%

“…Metastasis of the tumor cells through the extracellular matrix and basement membrane is associated with the production of MMP 24–26 . It is reported that rate of metastasis of tumor cells is directly related with the expression of MMPs in the cells 24,27,28 . In the current study, tretinoin treatment led to a prominent reduction in MMP‐2 and MMP‐9 expression in HT‐3 cervical cancer cells in dose‐dependent manner.…”

Section: Discussionsupporting

confidence: 50%

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Protective effect of tretinoin on cervical cancer growth and proliferation through downregulation of pFAK2 expression

Gong,

Zhao,

Liu

2024

Environmental Toxicology

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BackgroundCervical cancer, a life‐threatening disease, is the seventh most commonly detected cancer among women throughout the world. The present study investigated the effect of tretinoin on cervical cancer growth and metastasis in vitro and in vivo in the mice model.Materials and MethodsCell Counting Kit‐8, clonogenic survival, and transwell chamber assays were used for determination cells proliferation, colony formation, and invasiveness. Western blotting assay was used for assessment of protein expression whereas AutoDock Vina and Discovery studio software for in silico studies.ResultsTretinoin treatment significantly (p < .05) reduced the proliferation of HT‐3 and Caski cells in concentration‐based manner. Incubation with tretinoin caused a significant decrease in clonogenic survival of HT‐3 and Caski cells compared with the control cultures. The invasive potential of HT‐3 cells was decreased to 18%, whereas that of Caski cells to 21% on treatment with 8 μM concentration of tretinoin. In HT‐3 cells, tretinoin treatment led to a prominent reduction in p‐focal adhesion kinase (FAK), matrix metalloproteinases (MMP)‐2, and MMP‐9 expression in HT‐3 cells. Treatment of the cervical cancer mice model with tretinoin led to a prominent decrease in tumor growth. The metastasis of tumor in model cervical cancer mice group was effectively inhibited in spleen, intestines, and peritoneal cavity. In silico studies showed that tretinoin interacts with alanine, proline, isoleucine, and glycine amino acid residues of FAK protein to block its activation. The 2‐dimensional diagram of interaction of tretinoin with FAK protein revealed that tretinoin binds to alanine and glycine amino acids through conventional hydrogen bonding.ConclusionIn summary, tretinoin suppressed the proliferation, colony formation, and invasiveness of cervical cancer cells in vitro. It decreased the expression of activated focal adhesion kinase, MMP‐2, and MMP‐9 in HT‐3 cells in dose‐dependent manner. In silico studies showed that tretinoin interacts with alanine and glycine amino acids through conventional hydrogen bonding. In vivo data demonstrated that treatment of the cervical cancer mice model with tretinoin led to a prominent decrease in tumor growth. Therefore, tretinoin can be developed as an effective therapeutic agent for cervical cancer treatment.

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Section: Discussionsupporting

confidence: 55%

Section: Discussionsupporting

confidence: 50%

Protective effect of tretinoin on cervical cancer growth and proliferation through downregulation of pFAK2 expression

Gong,

Zhao,

Liu

2024

Environmental Toxicology

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“…By contrast, downregulation of MSK1 caused completely opposite consequences compared to the control cells (Figures 3 A and B). Previous studies have shown that matrix metalloproteinase-2 (MMP2) and MMP9 promoted tumor invasion and metastasis by degrading extracellular matrices [31,32]; thus the protein expression of MMP2 and MMP9 were assessed. The results suggested that MMP2 and MMP9 expression levels were increased by overexpression of MSK1 and decreased by MSK1 knockdown in OCM-1A and MUM-2C cell lines (Figure 3 C).…”

Section: Msk1 Promotes Uveal Melanoma Cell Metastasismentioning

confidence: 99%

MSK1 promotes cell proliferation and metastasis in uveal melanoma by phosphorylating CREB

Liu¹,

Liu²,

Wang³

et al. 2020

aoms

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Introduction: Uveal melanoma is known as a frequent intraocular tumor, with high metastasis and poor prognosis. Mitogen-and stress-activated protein kinase 1 (MSK1) is a serine/threonine kinase that has been reported to be associated with tumor progression in several types of human cancer. However, the role of MSK1 has rarely been studied in uveal melanoma and the underlying mechanism remained unclear. Material and methods: The expression level of MSK1 in human uveal melanoma tissues and normal uveal tissues was determined by qRT-PCR analysis, western blotting and immunohistochemistry (IHC). Subsequently, MTT assay, colony formation assay and flow cytometry assay were performed to assess the effects of MSK1 on cell proliferation. Wound-healing and transwell chamber assays were adopted to clarify the role of MSK1 in cell metastasis. Finally, the function of MSK1 was confirmed in vivo in a tumor-bearing mouse model. Results: The expression levels of MSK1 and p-cyclic AMP-responsive element binding protein (CREB) were strongly up-regulated in human uveal melanoma tissues. MSK1 overexpression facilitated cell viability and clone formation, and promoted migration and invasion of uveal melanoma cells. However, mutation of cyclic AMP-responsive element binding protein (CREB) at Ser133 residues reversed the effect of MSK1 on uveal melanoma cell proliferation and metastasis. The in vivo experiment suggested that the tumor weight was lower and the tumor mass grew more slowly in the shMSK1 group as compared to the shNC group. Conclusions: MSK1 promotes proliferation and metastasis of uveal melanoma cells by phosphorylated CREB at Ser133 residues. Therefore, MSK1 could be a promising candidate for uveal melanoma therapy and especially has tremendous potential in the treatment of cancers in which the MSK1-CREB pathway is abnormally active.

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Collagen prolyl 4-hydroxylases modify tumor progression

Shi

Gao

Zhang

et al. 2021

ABBS

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Collagen is the main component of the extracellular matrix. Hydroxylation of proline residues on collagen, catalyzed by collagen prolyl 4-hydroxylase (C-P4H), is essential for the stability of the collagen triple helix. Vertebrate C-P4H is an α2β2 tetramer with three isoenzymes differing in the catalytic α-subunits, which are encoded by P4HA1, P4HA2, and P4HA3 genes. In contrast, β-subunit is encoded by a single gene P4HB. The expressions of P4HAs and P4HB are regulated by multiple cellular factors, including cytokines, transcription factors, and microRNAs. P4HAs and P4HB are highly expressed in many tumors and participate in cancer progression. Several inhibitors of P4HAs and P4HB have been confirmed to have anti-tumor effects, suggesting that targeting C-P4H is a feasible strategy for cancer treatment. Here, we summarize recent progresses on the function and expression of regulatory mechanisms of C-P4H in cancer progression and point out the potential development of therapeutic strategies in targeting C-P4H in the future.

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The role of matrix metalloproteinases in cancer progression, in particular metastasis

Cited by 3 publications

References 245 publications

Protective effect of tretinoin on cervical cancer growth and proliferation through downregulation of pFAK2 expression

Protective effect of tretinoin on cervical cancer growth and proliferation through downregulation of pFAK2 expression

MSK1 promotes cell proliferation and metastasis in uveal melanoma by phosphorylating CREB

Collagen prolyl 4-hydroxylases modify tumor progression

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