Inhibition of N-(4-hydroxyphenyl)retinamide-Induced Apoptosis in Breast Cancer Cells by Galectin-3

Choi, Jin Hyuk; Chun, Kyung–Hee; Raz, Avraham; Hong, Waun Ki; Lotan, Reuben

doi:10.4161/cbt.3.5.808

Cited by 26 publications

(23 citation statements)

References 28 publications

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“…In agreement with this finding other studies reported that Gal-3 imparts resistance to apoptosis in breast, bladder and prostate cancer (Choi et al, 2004;Oka et al, 2005;Wang et al, 2010), by Bcl-2 up-regulation and inhibition of Gal-3 induced caspase-3 activity (Wang et al, 2010). Another report showed that use of Pect-MCP as a blocker of cell surface Gal-3 could induce apoptosis in prostate cancer by suppression of MAPK pathway (Yan and Katz, 2010).…”

Section: Discussionsupporting

confidence: 77%

“…This characteristic is unique among galectins and may be responsible for the interest in Gal-3 as a target molecule (Elola et al, 2007).The anti-apoptotic function of Gal-3 has been well demonstrated in variety of human cancers, such as breast, bladder and prostate (Choi et al, 2004;Oka et al, 2005;Wang et al, 2010). It has been demonstrated that Gal-3 knockout in PC3 prostate cancer cells could sensitize cells to chemotherapeutic drugs (Wang et al, 2010).…”

Section: Synergistic Effects Of Pectasol-c Modified Citrus Pectin An mentioning

confidence: 99%

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Synergistic Effects of PectaSol-C Modified Citrus Pectin an Inhibitor of Galectin-3 and Paclitaxel on Apoptosis of Human SKOV-3 Ovarian Cancer Cells

Hossein

Keshavarz²,

Ahmadi³

et al. 2013

Asian Pacific Journal of Cancer Prevention

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Section: Discussionsupporting

confidence: 77%

Section: Synergistic Effects Of Pectasol-c Modified Citrus Pectin An mentioning

confidence: 99%

Synergistic Effects of PectaSol-C Modified Citrus Pectin an Inhibitor of Galectin-3 and Paclitaxel on Apoptosis of Human SKOV-3 Ovarian Cancer Cells

Hossein

Keshavarz²,

Ahmadi³

et al. 2013

Asian Pacific Journal of Cancer Prevention

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“…Galectin-3 also demonstrates anti-apoptotic activity in response to retinoids [131]. This property of galectin-3 is consistent with its antiapoptotic function in T lymphocytes.…”

Section: Breast Cancer Cellssupporting

confidence: 57%

Galectin-3 and Regulation of Cell Function

Hsu

Kuwabara

Liu³

2005

Transfus Med Hemother

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The galectin family is phylogenically conserved in metazoans, presently consisting of 14 identified members in mammals, and galectin-3 is one of the most abundant, widely distributed, and well-studied members. It is present intracellularly in nuclear and cytoplasmic compartments, but is also secreted through an unconventional mechanism that involves vesicles and exosomes and, consequently, present outside the cell. While galectin-3 shares many features with other galectins, including cellular compartmentalization and functions, it appears to be unique in its structural constituency in the N-terminal domain, which is rich in proline, glycine, and alanine. It is through this domain that galectin-3 is able to form oligomers, and this may be one feature that functionally differentiates it from other galectins. Galectin-3 has been associated with several intracellular and extracellular functions, and recent investigations have uncovered proteins through which this lectin mediates its activities. The availability of targeted mutant mice deficient in galectin- 3 and other proteins has also contributed to our appreciation of the breadth of processes in which this protein is involved. Among cell functions attributable to galectin-3 are some that are associated with neoplastic transformation and invasiveness, but the most extensively documented ones are those related to the immune and inflammatory responses.

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“…These include the mitochondrial-mediated effector mechanism (intrinsic) and the death receptor-mediated (e.g., tumor necrosis factor (TNF) receptor and Fas) effector mechanism (extrinsic) [ [194,207] N.D. N.D. Breast Carcinoma [94, 109, 111, 123-126, 138, 172, 192, 208, 209] Intrinsic [109,111,172,192] Ceramide [94,138], Nitric Oxide [123][124][125][126], Oxidative Stress [109], ROS [111,172], and Bcl-2 Family [192] Breast Epithelial (Transformed) [210] N . D .…”

Section: Apoptosis Pathways and Their Regulatory Intermediatesmentioning

confidence: 99%

Mechanisms of fenretinide-induced apoptosis

Hail¹,

2006

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Fenretinide, a synthetic retinoid, has emerged as a promising anticancer agent based on numerous in vitro and animal studies, as well as chemoprevention clinical trials. In vitro observations suggest that the anticancer activity of fenretinide may arise from its ability to induce apoptosis in tumor cells. Diverse signaling molecules including reactive oxygen species, ceramide, and ganglioside GD3 can mediate apoptosis induction by fenretinide in transformed, premalignant, and malignant cells. In many cell types, these signaling intermediates appear to be induced by mechanisms that are independent of retinoic acid receptor activation, and ultimately initiate the intrinsic or mitochondrial-mediated pathway of cell elimination. Numerous investigations conducted during the past 10 years have discovered a great deal about the apoptogenic activity of fenretinide. In this review we explore the mechanisms associated with fenretinide-induced apoptosis and highlight certain mechanistic underpinnings of fenretinide-induced cell death that remain poorly understood and thus warrant further characterization.

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Inhibition of N-(4-hydroxyphenyl)retinamide-Induced Apoptosis in Breast Cancer Cells by Galectin-3

Cited by 26 publications

References 28 publications

Synergistic Effects of PectaSol-C Modified Citrus Pectin an Inhibitor of Galectin-3 and Paclitaxel on Apoptosis of Human SKOV-3 Ovarian Cancer Cells

Synergistic Effects of PectaSol-C Modified Citrus Pectin an Inhibitor of Galectin-3 and Paclitaxel on Apoptosis of Human SKOV-3 Ovarian Cancer Cells

Galectin-3 and Regulation of Cell Function

Mechanisms of fenretinide-induced apoptosis

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