CD55 in cancer: Complementing functions in a non-canonical manner

Bharti, Rashmi; Dey, Goutam; Lin, Feng; Lathia, Justin D.; Reizes, Ofer

doi:10.1016/j.canlet.2022.215935

Cited by 20 publications

(13 citation statements)

References 88 publications

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“…Moving forward it will be paramount to confirm MAC development in both our fH and CD55 knockdown cells to verify the mechanism through which tumor growth is inhibited. Similarly, CD55 has been shown to be elevated in many cancers, including in human lung cancer ( 47 ), and has been previously shown to promote tumorigenesis by increasing cell survival and proliferation pathways independent of the complement pathway, by leading to activation of pathways including, but not limited to SRC, NF-κB, MAPK, JNK, and JAK/STAT ( 48 ). While we did not observe any effects of CD55 silencing on cell proliferation, additional studies are required to examine effects of CD55 on other signaling pathways.…”

Section: Discussionmentioning

confidence: 99%

Upregulation of complement proteins in lung cancer cells mediates tumor progression

Kleczko

Poczobutt²,

Navarro³

et al. 2023

Front. Oncol.

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IntroductionIn vivo, cancer cells respond to signals from the tumor microenvironment resulting in changes in expression of proteins that promote tumor progression and suppress anti-tumor immunity. This study employed an orthotopic immunocompetent model of lung cancer to define pathways that are altered in cancer cells recovered from tumors compared to cells grown in culture.MethodsStudies used four murine cell lines implanted into the lungs of syngeneic mice. Cancer cells were recovered using FACS, and transcriptional changes compared to cells grown in culture were determined by RNA-seq.ResultsChanges in interferon response, antigen presentation and cytokine signaling were observed in all tumors. In addition, we observed induction of the complement pathway. We previously demonstrated that activation of complement is critical for tumor progression in this model. Complement can play both a pro-tumorigenic role through production of anaphylatoxins, and an anti-tumorigenic role by promoting complement-mediated cell killing of cancer cells. While complement proteins are produced by the liver, expression of complement proteins by cancer cells has been described. Silencing cancer cell-specific C3 inhibited tumor growth In vivo. We hypothesized that induction of complement regulatory proteins was critical for blocking the anti-tumor effects of complement activation. Silencing complement regulatory proteins also inhibited tumor growth, with different regulatory proteins acting in a cell-specific manner.DiscussionBased on these data we propose that localized induction of complement in cancer cells is a common feature of lung tumors that promotes tumor progression, with induction of complement regulatory proteins protecting cells from complement mediated-cell killing.

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Section: Discussionmentioning

confidence: 99%

Upregulation of complement proteins in lung cancer cells mediates tumor progression

Kleczko

Poczobutt²,

Navarro³

et al. 2023

Front. Oncol.

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“…The CD55 signaling can be activated by growth factors, cytokines, and augment prostaglandins [43]. In Hep3B hepatoma cells, the exposition of cytokines such as TNF-α, IL-6, and IL-1β increased the expression of CD55 (three-fold) and CD59 (twofold) and decreased the expression of CD46, demonstrating the relevance function of TME and inflammatory cytokines on the expression of mCRP [51].…”

Section: Cd55mentioning

confidence: 92%

“…CD55, also known as Decay-accelerating factor (DAF), was first discovered in 1969 on the cell surface of an erythrocyte. It is a glycophosphatidylinositol (GPI)-anchored cell surface glycoprotein with a molecular weight that varies from between 50 and 100 kDa depending on cell type [43]. DAF is present in most cell types; its gene is encoded on chromosome 1q32.2 located adjacent to the genes comprising the RCA gene family, which includes as well CD46.…”

Section: Cd55mentioning

confidence: 99%

“…Has been reported that cell-surface CD55 is a ligand for CD97, a member of the epidermal growth factor seven-span transmembrane (EGF-7TM) receptor family; the binding of CD55 to CD97 can protect several cell types from complement-mediated damage, thus playing an important role in host defense and inflammation [43,49]. Furthermore, CD55 can stimulate CD97 signaling and modulate cancer metastasis, as a mechanism dependent on the upregulation of MMP2 and MMP9 [50].…”

Section: Cd55mentioning

confidence: 99%

“…But these proteins also can regulate non-complement signaling in promoting cancer proliferation, chemoresistance, and metastasis. We proposed a model of signaling pathways activated by mCRP [12] and recently Bharti et al also proposed a series of pathways intracellularly by CD55 [43]. Due to their relevance in the potential of anticancer antibodies, they have been proposed and studied mCRP as therapeutic targets through various models and strategies: small interfering RNAs (siRNA) [69,71,84,85], antibodies anti-mCRP [13], and enzyme-peptide [13,86].…”

Section: Therapeutic Strategies and Future Challenges To Regulate Mcr...mentioning

confidence: 99%

See 2 more Smart Citations

Membrane-Bound Complement Regulatory Proteins in Breast Cancer: Are They Best Therapeutic Targets?

Álvarez-Lorenzo¹,

Montalvo-Castro²,

Jiménez-López³

et al. 2023

Breast Cancer Updates

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Breast cancer is one of the most aggressive diseases in women, responsible for thousands of deaths annually and millions of new diagnoses; its treatment presents multiple obstacles due to late diagnosis and the various mechanisms of tumor resistance. In breast cancer the membrane-bound complement regulatory proteins (mCRP) have been proposed as biomarkers of malignant cellular transformation. These are molecules capable of inhibiting therapeutic efficacy, from both antibodies and cytotoxic drugs. Therefore, these proteins are potential targets to increase therapeutic efficacy and avoid cancer progression. We will gather information about mCRP: (i) structural features; (ii) expression levels in breast cancer and relationship with prognosis; (iii) therapeutic resistance mechanisms; and (iv) strategies to down-regulate mCRP in both activity and expression.

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Immune cells mediate the causal pathway linking circulating complements to cancer: A Mendelian randomization study

Pan,

Jing

2024

Inflamm. Res.

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CD55 in cancer: Complementing functions in a non-canonical manner

Cited by 20 publications

References 88 publications

Upregulation of complement proteins in lung cancer cells mediates tumor progression

Upregulation of complement proteins in lung cancer cells mediates tumor progression

Membrane-Bound Complement Regulatory Proteins in Breast Cancer: Are They Best Therapeutic Targets?

Immune cells mediate the causal pathway linking circulating complements to cancer: A Mendelian randomization study

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