Caveolin‐1 contributes to anoikis resistance in human gastric cancer SGC‐7901 cells via regulating Src‐dependent EGFR‐ITGB1 signaling

Wang, Ke; Zhu, Xue; Mei, Dan; Ding, Zhongyang

doi:10.1002/jbt.22202

Cited by 16 publications

(17 citation statements)

References 22 publications

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“…Indeed, CAV1 is reported to increase resistance to anoikis, which may be related to Cav1's role in neuroprotection. 65 , 66 Because the changed proteins were not significantly enriched in immune functions or pathways with this analysis, we cannot rule out the possibility that the immune effects of Cav1 KO may be indirect and due to alterations in the structure of the plasma membrane. This may, in fact, reconcile why some studies observe a pro- or anti-inflammatory effect, because a change in membrane dynamics could affect both.…”

Section: Resultsmentioning

confidence: 95%

Neuroretinal-Derived Caveolin-1 Promotes Endotoxin-Induced Inflammation in the Murine Retina

Gurley

Gmyrek

McClellan

et al. 2020

Invest. Ophthalmol. Vis. Sci.

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Purpose The immune-privileged environment and complex organization of retinal tissue support the retina's essential role in visual function, yet confound inquiries into cell-specific inflammatory effects that lead to dysfunction and degeneration. Caveolin-1 (Cav1) is an integral membrane protein expressed in several retinal cell types and is implicated in immune regulation. However, whether Cav1 promotes or inhibits inflammatory processes in the retina (as well as in other tissues) remains unclear. Previously, we showed that global-Cav1 depletion resulted in reduced retinal inflammatory cytokine production but paradoxically elevated retinal immune cell infiltration. We hypothesized that these disparate responses are the result of differential cell-specific Cav1 functions in the retina. Methods We used Cre/lox technology to deplete Cav1 specifically in the neural retinal (NR) compartment to clarify the role NR-specific Cav1 (NR-Cav1) in the retinal immune response to intravitreal inflammatory challenge induced by activation of Toll-like receptor-4 (TLR4). We used multiplex protein suspension array and flow cytometry to evaluate innate immune activation. Additionally, we used bioinformatics assessment of differentially expressed membrane-associated proteins to infer relationships between NR-Cav1 and immune response pathways. Results NR-Cav1 depletion, which primarily affects Müller glia Cav1 expression, significantly altered immune response pathway regulators, decreased retinal inflammatory cytokine production, and reduced retinal immune cell infiltration in response to LPS-stimulated inflammatory induction. Conclusions Cav1 expression in the NR compartment promotes the innate TLR4-mediated retinal tissue immune response. Additionally, we have identified novel potential immune modulators differentially expressed with NR-Cav1 depletion. This study further clarifies the role of NR-Cav1 in retinal inflammation.

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Section: Resultsmentioning

confidence: 95%

Neuroretinal-Derived Caveolin-1 Promotes Endotoxin-Induced Inflammation in the Murine Retina

Gurley

Gmyrek

McClellan

et al. 2020

Invest. Ophthalmol. Vis. Sci.

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“…Many of these shared PPIs (e.g., EGF/ epidermal growth factor, SRC/neuronal proto-oncogene tyrosine-protein kinase, BCAR1/breast cancer anti-estrogen resistance protein 1) are also associated with anoikis (programmed cell death upon detachment from the extracellular matrix). Indeed, CAV1 has been reported to increase resistance to anoikis, which may be related to Cav1's role in neuroprotection (45,46). But because the changed proteins were not significantly enriched in immune functions or pathways, we cannot rule out the possibility that the immune effects of Cav1 KO may be indirect and due to alterations in the structure of the plasma membrane.…”

Section: Immunomodulatory Traf3 Protein Is Highly Expressed In Retinamentioning

confidence: 91%

Neuroretinal-derived caveolin-1 promotes endotoxin-induced inflammation in the murine retina

Gurley

Gmyrek

McClellan

et al. 2020

Preprint

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Chronic ocular inflammation is associated with many retinal degenerative diseases that result in vision loss. The immune-privileged environment and complex organization of retinal tissue allow for the retina’s essential role in visual function processes, yet confound inquiries into cell-specific inflammatory effects that lead to retinal dysfunction and degeneration. Caveolin-1 (Cav1) is an integral membrane protein expressed in many retinal cell populations and has been implicated in retinal immune regulation. However, the direction (i.e., promotion or inhibition) in which Cav1 regulates inflammatory processes in the retina (as well as in other tissues) remains unclear. Previously, we showed that global-Cav1 depletion in the retina paradoxically resulted in reduced retinal inflammatory cytokine production with concurrent elevated retinal immune cell infiltration. We hypothesized that our previous results could be explained by cell-specific Cav1 functions in the retina. Here, we utilized our Chx10 (visual system homeobox 2)-Cre knockout model to deplete Cav1 specifically in the neural retinal (NR) compartment in order to clarify the role of neural retinal-specific Cav1 (NR-Cav1) in the retinal immune response to intravitreal LPS (lipopolysaccharide) challenge. Our data support that neural retinal-derived Cav1 promotes retinal tissue inflammation as Chx10-mediated Cav1 depletion was sufficient to suppress both retinal cytokine production and immune cell infiltration following inflammatory stimulation. Additionally, we identify Traf3 (tumor necrosis factor (TNF) receptor-associated factor 3) as a highly expressed potential immune modulator in retinal tissue that is upregulated with NR-Cav1 depletion. Furthermore, this study highlights the importance for understanding the role of Cav1 (and other proteins) in cell-specific contexts.

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“…The expression of CAV1 is higher in cancer compared to benign tissue and correlates with poor prognosis [127]. The overexpression of CAV1 is associated with increased cell survival, anchorageindependent growth, and epithelial-mesenchymal transition, migration, invasion, and resistance to anti-neoplastic drugs [38,94,111,127,176].…”

Section: Cav1 As a Tumor Suppressor Or Promotermentioning

confidence: 99%

“…Additional evidence places CAV1 at mitochondria-ER interphase sites (localizing CAV1 indirectly to mitochondria), referred to as mitochondria-associated ER membranes (MAMs), as well as lysosomal, peroxisomal, and exosomal membranes, as will be discussed in this review Src in focal adhesions [50]. In metastatic gastric cancer cells, CAV1 promotes resistance to anoikis in a Src-dependent manner by activation of the EGFR/integrin βI, PI3K/pAkt, and MEK/ERK signaling pathways [176]. In addition, in hepatocellular cancer cell lines, CAV1 is required for the induction of survival via the TGF-β/EGFR/pAkt signaling pathway [111].…”

Section: Cav1 As a Tumor Suppressor Or Promotermentioning

confidence: 99%

Caveolin-1 function at the plasma membrane and in intracellular compartments in cancer

Simón

Campos

Leyton

et al. 2020

Cancer Metastasis Rev

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Caveolin-1 (CAV1) is commonly considered to function as a cell surface protein, for instance in the genesis of caveolae. Nonetheless, it is also present in many intracellular organelles and compartments. The contributions of these intracellular pools to CAV1 function are generally less well understood, and this is also the case in the context of cancer. This review will summarize literature available on the role of CAV1 in cancer, highlighting particularly our understanding of the canonical (CAV1 in the plasma membrane) and non-canonical pathways (CAV1 in organelles and exosomes) linked to the dual role of the protein as a tumor suppressor and promoter of metastasis. With this in mind, we will focus on recently emerging concepts linking CAV1 function to the regulation of intracellular organelle communication within the same cell where CAV1 is expressed. However, we now know that CAV1 can be released from cells in exosomes and generate systemic effects. Thus, we will also elaborate on how CAV1 participates in intracellular communication between organelles as well as signaling between cells (non-canonical pathways) in cancer.

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Caveolin‐1 contributes to anoikis resistance in human gastric cancer SGC‐7901 cells via regulating Src‐dependent EGFR‐ITGB1 signaling

Cited by 16 publications

References 22 publications

Neuroretinal-Derived Caveolin-1 Promotes Endotoxin-Induced Inflammation in the Murine Retina

Neuroretinal-Derived Caveolin-1 Promotes Endotoxin-Induced Inflammation in the Murine Retina

Neuroretinal-derived caveolin-1 promotes endotoxin-induced inflammation in the murine retina

Caveolin-1 function at the plasma membrane and in intracellular compartments in cancer

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