Retinoic Acid-Induced Golgi Apparatus Disruption in F2000 Fibroblasts: A Model for Enhanced Intracellular Retrograde Transport

Tzankov, Alexandar

doi:10.5483/bmbrep.2003.36.3.265

Cited by 3 publications

(4 citation statements)

References 25 publications

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“…1997), but structural alterations may also be caused by several pharmacological agents, such as RA (Wu et al. 1994; Dinter and Berger 1998; Tzankov 2003; Selinummi et al. 2006b).…”

Section: Discussionmentioning

confidence: 99%

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Cholesterol supports the retinoic acid‐induced synaptic vesicle formation in differentiating human SH‐SY5Y neuroblastoma cells

Sarkanen

Nykky

Siikanen

et al. 2007

Journal of Neurochemistry

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Synaptic vesicle formation, vesicle activation and exo/endocytosis in the pre-synaptic area are central steps in neuronal communication. The formation and localization of synaptic vesicles in human SH-SY5Y neuroblastoma cells, differentiated with 12-o-tetradecanoyl-phorbol-13-acetate, dibutyryl cyclic AMP, all-trans-retinoic acid (RA) and cholesterol, was studied by fluorescence microscopy and immunocytochemical methods. RA alone or together with cholesterol, produced significant neurite extension and formation of cell-to-cell contacts. Synaptic vesicle formation was followed by anti-synaptophysin (SypI) and AM1-43 staining. SypI was only weakly detected, mainly in cell somata, before 7 days in vitro, after which it was found in neurites. Depolarization of the differentiated cells with high potassium solution increased the number of fluorescent puncta, as well as SypI and AM1-43 co-localization. In addition to increase in the number of synaptic vesicles, RA and cholesterol also increased the number and distribution of lysosome-associated membrane protein 2 labeled lysosomes. RA-induced Golgi apparatus fragmentation was partly avoided by co-treatment with cholesterol. The SH-SY5Y neuroblastoma cell line, differentiated by RA and cholesterol and with good viability in culture, is a valuable tool for basic studies of neuronal metabolism, specifically as a model for dopaminergic neurons.

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“…1997), but structural alterations may also be caused by several pharmacological agents, such as RA (Wu et al. 1994; Dinter and Berger 1998; Tzankov 2003; Selinummi et al. 2006b).…”

Section: Discussionmentioning

confidence: 99%

“…RA and cholesterol have previously been suggested to be involved in increasing the lysosomal activity (Kang et al. 1998; Tzankov 2003; Zheng et al. 2006).…”

Section: Discussionmentioning

confidence: 99%

Cholesterol supports the retinoic acid‐induced synaptic vesicle formation in differentiating human SH‐SY5Y neuroblastoma cells

Sarkanen

Nykky

Siikanen

et al. 2007

Journal of Neurochemistry

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“…Although further investigation is required to delineate the mechanism for the RA effect, we suggest that one possibility is that RA binds to RBP (28) and affects interaction with the putative receptor; interestingly, in the context of TTR and RA inhibition of RBP endocytosis, RA binding influences a region on the RBP surface that is also involved in TTR binding (29). An alternative possibility for the RA influence on RBP endocytic transport is RAdependent biophysical membrane changes at the cell surface (30,31); in the context of cellular transport, for example, it has been reported that 9-cis RA can affect the process of phagocytosis (32).…”

Section: Discussionmentioning

confidence: 99%

Evidence for a specific cell membrane retinol-binding protein transport mechanism in a human keratinocyte line

Huang

Vieira²

2006

Int J Mol Med

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Abstract. The epidermis is highly sensitive to retinoids, and vitamin A (retinol) is a critical factor in the regulation of skin cell differentiation and proliferation. Despite extensive knowledge of retinoid-mediated gene transcription effects on epidermal cells and evidence for retinoid-mediated suppression of carcinogenesis in skin, basic transport events, especially cellular uptake, of this vitamin remain poorly understood and controversial. Herein, evidence is presented for receptormediated uptake of retinol-binding protein, RBP, the specific circulatory vitamin A carrier, in the A431 human epidermal cell line. Cellular RBP uptake was significantly inhibited by anti-RBP IgG. Addition of transthyretin (TTR), a circulatory protein that can interact with RBP, to the internalization assay also significantly reduced RBP uptake to 49.4±4.6% (± SEM) of control values (p<0.01). RBP uptake was impaired by sucrose, a known inhibitor of early endocytosis, but not significantly affected by a disruptor of later trafficking events, chlorpromazine. Binding analysis indicated saturable RBP binding to the cell surface and a total of about 94,000 binding sites/cell. Based on dissociation constants, two RBP binding sites were detected with a 50-fold affinity difference: 0.7 and 35.0 nM, with 12,000 and 82,000 receptors/cell, respectively. These results indicate that high affinity RBP receptors capable of internalizing RBP independently of TTR exist in these malignant keratinocytes, and that TTR influences binding of RBP to its putative receptor(s). Overall, the data establish membrane transport parameters for RBP, and provide a basis for examining modulation of vitamin A endocytosis that may accompany changes in proliferation or differentiation state of epidermal cells.

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“…RA is an anti-metastatic drug that interferes with the function of the Golgi apparatus [32]. Given that most proteins related to cancer metastasis are glycosylated on the Golgi apparatus [33], its destruction should inhibit metastasis.…”

Section: Inhibition Of Cell Migration In Vitromentioning

confidence: 99%

Chondroitin Sulfate-Modified Liposomes for Targeted Co-Delivery of Doxorubicin and Retinoic Acid to Suppress Breast Cancer Lung Metastasis

Zhang

Luo

2021

Pharmaceutics

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Breast cancer treatment remains challenging due to high levels of cell metastasis. Chemotherapy drug combinations can inhibit both tumor growth in situ and metastasis to distant organs. Therefore, here, we developed chondroitin sulfate liposomes (CSLs) as a carrier for the co-delivery of retinoic acid (RA) and doxorubicin (DOX) and examined their efficiency in suppressing lung metastasis of breast cancer. CSLs were prepared using CS–deoxycholic acid conjugates and found to encapsulate both RA and DOX via hydrophobic and hydrophilic interactions. The resulting DOX+RA-CSLs were uniformly spherical and showed good serum stability and encapsulation efficiency of 98.7% ± 1.3% for RA and 90.8% ± 2.9% for DOX. Pharmacodynamic experiments in vitro and in vivo also revealed that DOX+RA-CSLs had better anticancer and anti-metastatic activity than CS-free liposomes, single drug-loaded liposomes, and free drug solutions at the same dose (2 mg/kg DOX or RA). Our results suggest that this liposomal delivery system can effectively suppress lung metastasis of breast cancer.

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Retinoic Acid-Induced Golgi Apparatus Disruption in F2000 Fibroblasts: A Model for Enhanced Intracellular Retrograde Transport

Cited by 3 publications

References 25 publications

Cholesterol supports the retinoic acid‐induced synaptic vesicle formation in differentiating human SH‐SY5Y neuroblastoma cells

Cholesterol supports the retinoic acid‐induced synaptic vesicle formation in differentiating human SH‐SY5Y neuroblastoma cells

Evidence for a specific cell membrane retinol-binding protein transport mechanism in a human keratinocyte line

Chondroitin Sulfate-Modified Liposomes for Targeted Co-Delivery of Doxorubicin and Retinoic Acid to Suppress Breast Cancer Lung Metastasis

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