Prohibitin-2 Binding Modulates Insulin-like Growth Factor-binding Protein-6 (IGFBP-6)-induced Rhabdomyosarcoma Cell Migration

Fu, Ping; Yang, Zhiyong; Bach, Leon Ashley

doi:10.1074/jbc.m113.510826

Cited by 50 publications

(54 citation statements)

References 58 publications

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“…We also found peptide sequences from histones (including histones H1.2, H2B, and H4), heat shock protein 70, ribosomal proteins (40S and 60S), and PARP1, as well as Prohibitin-2 and myristoylated alaninerich protein kinase C substrate (MARCK), which have putative roles in invasion and metastasis ( Fig. 1, Table 1) (8,(22)(23)(24). The most striking ATDC-interacting protein identified by this screen was RNF8 (37% peptide coverage by mass spectroscopy, Fig.…”

Section: Atdc Bindsmentioning

confidence: 99%

ATDC (Ataxia Telangiectasia Group D Complementing) Promotes Radioresistance through an Interaction with the RNF8 Ubiquitin Ligase

Yang

Palmbos

Wang

et al. 2015

Journal of Biological Chemistry

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Background: ATDC/TRIM29 promotes resistance to ionizing radiation, but the factor(s) that mediate this effect are incompletely understood. Results: ATDC/TRIM29 binds to RNF8, promoting DNA repair and resistance to IR. Conclusion: Following DNA damage, ATDC/TRIM29 is phosphorylated and interacts with RNF8, promoting DNA repair and cell survival. Significance: The interaction between ATDC/TRIM29 and RNF8 is novel and is important for the DNA damage response.

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Section: Atdc Bindsmentioning

confidence: 99%

ATDC (Ataxia Telangiectasia Group D Complementing) Promotes Radioresistance through an Interaction with the RNF8 Ubiquitin Ligase

Yang

Palmbos

Wang

et al. 2015

Journal of Biological Chemistry

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“…If and how such direct effects of IGFBPs impact on cell metabolism remains to be established. Intriguingly, one of the recognized IGFBP‐6 receptor is prohibitin‐2 (PBH2) 57, 58. Although PBH2 is located as a single transmembrane helix spanning protein in the cell membrane, the majority of PBH2 is located in a ring‐shaped oligomer in the inner mitochondrial membrane where it functions as a crucial mitophagy receptor 57.…”

Section: Igfs and Igfbp‐6 Have Multiple Important Functionsmentioning

confidence: 99%

“…These results raised the possibility that a receptor or membrane protein may be involved. It was further demonstrated that prohibitin‐2 (PBH2) binds IGFBP‐6 on the cell surface of RMS cells 58. Although PBH2 was indispensable for IGFBP‐6‐induced cell migration, this action was not dependent on MAPK activation.…”

Section: Cell Migration and Chemotaxis In Tumour Microenvironmentmentioning

confidence: 99%

From fever to immunity: A new role for IGFBP‐6?

Liso

Capitanio

Gerli

et al. 2018

J Cellular Molecular Medi

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Fever is a fundamental response to infection and a hallmark of inflammatory disease, which has been conserved and shaped through millions of years of natural selection. Although fever is able to stimulate both innate and adaptive immune responses, the very nature of all the molecular thermosensors, the timing and the detailed mechanisms translating a physical trigger into a fundamental biological response are incompletely understood. Here we discuss the consequence of hyperthermic stress in dendritic cells (DCs), and how the sole physical input is sensed as an alert stimulus triggering a complex transition in a very narrow temporal window. Importantly, we review recent findings demonstrating the significant and specific changes discovered in gene expression and in the metabolic phenotype associated with hyperthermia in DCs. Furthermore, we discuss the results that support a model based on a thermally induced autocrine signalling, which rewires and sets a metabolism checkpoint linked to immune activation of dendritic cells. Importantly, in this context, we highlight the novel regulatory functions discovered for IGFBP‐6 protein: induction of chemotaxis; capacity to increase oxidative burst and degranulation of neutrophils, ability to induce metabolic changes in DCs. Finally, we discuss the role of IGFBP‐6 in autoimmune disease and how novel mechanistic insights could lead to exploit thermal stress‐related mechanisms in the context of cancer therapy.

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“…127,128 Conversely, IGFBP-6 promotes cell migration in rhabdomyosarcoma and colon cancer cells independent of IGF-2, an action mediated by p38, pERK, JNK1 signaling pathways. 129–131 Evaluation of the role of IGFBP-6 in ovarian cancer decreased migration of HEY cells, an aggressive ovarian cancer cell line, whereas in less aggressive cultures such as SKOV3, IGFBP-6 stimulated cell migration. 132 Although IGFBP-6 induced phosphorylation of ERK and JNK in both cell lines, exposure to inhibitors of ERK and JNK only reduced the migration of HEY cells.…”

Section: Igf Axis and Triple-negative Breast Cancermentioning

confidence: 99%

“…132 This suggests that IGFBP-6 has the potential to reduce metastasis independent of IGF-2. 128–131 Under hypoxic conditions, IGFBP-6 also inhibits angiogenesis independent of IGF-2 in vitro and in vivo . 128 Concurrently, IGFBP-6 has the ability to induce cell migration by binding directly to prohibin-2 (PHB2), a single-span membrane protein.…”

Section: Igf Axis and Triple-negative Breast Cancermentioning

confidence: 99%

Estrogen Receptor-β and the Insulin-Like Growth Factor Axis as Potential Therapeutic Targets for Triple-Negative Breast Cancer

Hamilton¹,

Márquez-Garbán

Mah

et al. 2015

Crit Rev Oncog

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Triple-negative breast cancers (TNBCs) lack estrogen receptor-α (ERα), progesterone receptor (PR), and human epidermal growth factor receptor-2 (HER2) amplification and account for almost half of all breast cancer deaths. This breast cancer subtype largely affects women who are premenopausal, African-American, or have BRCA1/2 mutations. Women with TNBC are plagued with higher rates of distant metastasis that significantly diminish their overall survival and quality of life. Due to their poor response to chemotherapy, patients with TNBC would significantly benefit from development of new targeted therapeutics. Research suggests that the insulin-like growth factor (IGF) family and estrogen receptor beta-1 (ERβ1), due to their roles in metabolism and cellular regulation, might be attractive targets to pursue for TNBC management. Here, we review the current state of the science addressing the roles of ERβ1 and the IGF family in TNBC. Further, the potential benefit of metformin treatment in patients with TNBC as well as areas of therapeutic potential in the IGF-ERβ1 pathway are highlighted.

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Prohibitin-2 Binding Modulates Insulin-like Growth Factor-binding Protein-6 (IGFBP-6)-induced Rhabdomyosarcoma Cell Migration

Cited by 50 publications

References 58 publications

ATDC (Ataxia Telangiectasia Group D Complementing) Promotes Radioresistance through an Interaction with the RNF8 Ubiquitin Ligase

ATDC (Ataxia Telangiectasia Group D Complementing) Promotes Radioresistance through an Interaction with the RNF8 Ubiquitin Ligase

From fever to immunity: A new role for IGFBP‐6?

Estrogen Receptor-β and the Insulin-Like Growth Factor Axis as Potential Therapeutic Targets for Triple-Negative Breast Cancer

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