Effect of all-<i>trans</i>retinoic acid (ATRA) on syndecan-1 expression and its chemoprotective effect in benzo(α)pyrene-induced lung cancer mice model

Ramya, D.; Siddikuzzaman,; Grace, V. M. Berlin

doi:10.3109/08923973.2012.693086

Cited by 20 publications

(8 citation statements)

References 36 publications

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“…It is noted that myeloma and pancreatic chemotherapeutic drugs tend to induce accumulation of shed SDC-1 exactly as benzo(α)pyrene does in lung cancer. To avoid such tumor initiating effect, the use of metalloproteinase inhibitors in combination with chemotherapy and all-trans retinoic acid was suggested (153, 157). Another strategy to accomplish shedding inhibition involves the use of SST0001, a non-anticoagulant heparin with anti-heparanase activity, whose use diminishes the heparanase-induced SDC-1 shedding.…”

Section: Potential Syndecan-based Pharmacological Approaches In Cancementioning

confidence: 99%

Syndecans as Modulators and Potential Pharmacological Targets in Cancer Progression

et al. 2014

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Extracellular matrix (ECM) components form a dynamic network of key importance for cell function and properties. Key macromolecules in this interplay are syndecans (SDCs), a family of transmembrane heparan sulfate proteoglycans (HSPGs). Specifically, heparan sulfate (HS) chains with their different sulfation pattern have the ability to interact with growth factors and their receptors in tumor microenvironment, promoting the activation of different signaling cascades that regulate tumor cell behavior. The affinity of HS chains with ligands is altered during malignant conditions because of the modification of chain sequence/sulfation pattern. Furthermore, matrix degradation enzymes derived from the tumor itself or the tumor microenvironment, like heparanase and matrix metalloproteinases, ADAM as well as ADAMTS are involved in the cleavage of SDCs ectodomain at the HS and protein core level, respectively. Such released soluble SDCs “shed SDCs” in the ECM interact in an autocrine or paracrine manner with the tumor or/and stromal cells. Shed SDCs, upon binding to several matrix effectors, such as growth factors, chemokines, and cytokines, have the ability to act as competitive inhibitors for membrane proteoglycans, and modulate the inflammatory microenvironment of cancer cells. It is notable that SDCs and their soluble counterparts may affect either the behavior of cancer cells and/or their microenvironment during cancer progression. The importance of these molecules has been highlighted since HSPGs have been proposed as prognostic markers of solid tumors and hematopoietic malignancies. Going a step further down the line, the multi-actions of SDCs in many levels make them appealing as potential pharmacological targets, either by targeting directly the tumor or indirectly the adjacent stroma.

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Section: Potential Syndecan-based Pharmacological Approaches In Cancementioning

confidence: 99%

Syndecans as Modulators and Potential Pharmacological Targets in Cancer Progression

et al. 2014

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“…Syndecan-1 is a proteoglycan that mediates cell-cell adhesion and prevents invasion in epithelial cells. Retinoic acid may increase syndecan-1 expression to block invasion/metastasis of lung cancer [ 37 ]. Notably, retinoic acid has been found to reduce chemotherapy-induced neuropathy in an animal model as well as patients with lung cancer [ 38 ].…”

Section: Retinoic Acid and Lung Cancermentioning

confidence: 99%

Retinoic acid and cancer treatment

Chen¹,

Hsu²,

H³

et al. 2014

BioMed

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Retinoic acid which belongs to the retinoid class of chemical compounds is an important metabolite of vitamin A in diets. It is currently understood that retinoic acid plays important roles in cell development and differentiation as well as cancer treatment. Lung, prostate, breast, ovarian, bladder, oral, and skin cancers have been demonstrated to be suppressed by retinoic acid. Our results also show that low doses and high doses of retinoic acid may respectively cause cell cycle arrest and apoptosis of cancer cells. Also, the common cell cycle inhibiting protein, p27, and the new cell cycle regulator, Cdk5, are involved in retinoic acid’s effects. These results provide new evidence indicating that the molecular mechanisms of/in retinoic acid may control cancer cells’ fates. Since high doses of retinoic acid may lead to cytotoxicity, it is probably best utilized as a potential supplement in one’s daily diet to prevent or suppress cancer progression. In this review, we have collected numerous references demonstrating the findings of retinoic acid in melanoma, hepatoma, lung cancer, breast cancer, and prostate cancer. We hope these observations will shed light on the future investigation of retinoic acid in cancer prevention and therapy.

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“…All-trans retinoic acid, an active metabolite of retinal, has been shown to exert anticancer activity against different cancer cells. It has been reported that benzo(α)pyrene induces accumulation of shed SDC1 in lung cancer [ 155 ]. One study examined the level of SDC1 expression and the chemopreventive effect of all-trans retinoic acid in a benzo(α)pyrene-induced lung cancer model in BALB/c mice.…”

Section: Introductionmentioning

confidence: 99%

“…One study examined the level of SDC1 expression and the chemopreventive effect of all-trans retinoic acid in a benzo(α)pyrene-induced lung cancer model in BALB/c mice. The results indicated that all-trans retinoic acid inhibited lung tumor development and reduced SDC1 expression in cancer cells [ 155 ]. It has been reported that bFGF/FGF2 induces shedding of SDC1 in cancer cells [ 156 ].…”

Section: Introductionmentioning

confidence: 99%

Molecular and clinical profiles of syndecan-1 in solid and hematological cancer for prognosis and precision medicine

et al. 2015

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Syndecan-1 (SDC1, CD138) is a key cell surface adhesion molecule essential for maintaining cell morphology and interaction with the surrounding microenvironment. Deregulation of SDC1 contributes to cancer progression by promoting cell proliferation, metastasis, invasion and angiogenesis, and is associated with relapse through chemoresistance. SDC1 expression level is also associated with responses to chemotherapy and with prognosis in multiple solid and hematological cancers, including multiple myeloma and Hodgkin lymphoma. At the tissue level, the expression levels of SDC1 and the released extracellular domain of SDC1 correlate with tumor malignancy, phenotype, and metastatic potential for both solid and hematological tumors in a tissue-specific manner. The SDC1 expression profile varies among cancer types, but the differential expression signatures between normal and cancer cells in epithelial and stromal compartments are directly associated with aggressiveness of tumors and patient's clinical outcome and survival. Therefore, relevant biomarkers of SDC signaling may be useful for selecting patients that would most likely respond to a particular therapy at the time of diagnosis or perhaps for predicting relapse. In addition, the reciprocal expression signature of SDC between tumor epithelial and stromal compartments may have synergistic value for patient selection and the prediction of clinical outcome.

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Effect of all-transretinoic acid (ATRA) on syndecan-1 expression and its chemoprotective effect in benzo(α)pyrene-induced lung cancer mice model

Cited by 20 publications

References 36 publications

Syndecans as Modulators and Potential Pharmacological Targets in Cancer Progression

Syndecans as Modulators and Potential Pharmacological Targets in Cancer Progression

Retinoic acid and cancer treatment

Molecular and clinical profiles of syndecan-1 in solid and hematological cancer for prognosis and precision medicine

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