Type I insulin-like growth factor receptor signaling in hematological malignancies

Vishwamitra, Deeksha; George, Suraj Konnath; Shi, Ping; Kaseb, Ahmed O.; Amin, Hesham M.

doi:10.18632/oncotarget.12123

Cited by 42 publications

(40 citation statements)

References 293 publications

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“…FER kinase serves a central role in breast cancer metastasis and PCa cell proliferation (34). IGF serves key roles in the progression of different types of cancer, such as breast, prostate, lung, ovarian and skin cancer (35). The JAK2 signaling pathway is involved in cytokine signaling, which regulates hematopoietic cell development, cell metabolism and immune responses (36).…”

Section: Discussionmentioning

confidence: 99%

Knockdown of GSG2 inhibits prostate cancer progression in�vitro and in�vivo

Lin

et al. 2020

Int J Oncol

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Prostate cancer (PCa) is the second leading cause of cancer-related death among men worldwide. The present study aimed to investigate the role of germ cell-specific gene 2 protein (GSG2), also termed histone H3 phosphorylated by GSG2 at threonine-3, in the development and progression of PCa. GSG2 expression levels in PCa tissues and para-carcinoma tissues was detected by immunohistochemistry. The GSG2 knockdown cell model was constructed by lentivirus infection, and the knockdown efficiency was verified by qPCR and WB. In addition, the effects of shGSG2 on cell proliferation, colony formation and apoptosis were evaluated by Celigo cell counting assay, Giemsa staining and flow cytometry, respectively. Tumor development in nude mice was also detected. GSG2 expression was upregulated in PCa tissues and human PCa cell lines PC-3 and DU 145. High expression of GSG2 in tumor samples was associated with progressed tumors. GSG2 knockdown suppressed cell proliferation and colony formation, but promoted apoptosis, which was also verified in vivo.The results of the present study revealed that GSG2 upregulation was associated with PCa progression; GSG2 knockdown inhibited cell proliferation and colony formation and induced apoptosis, and may therefore serve as a potential therapeutic target for PCa therapy.

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Section: Discussionmentioning

confidence: 99%

Knockdown of GSG2 inhibits prostate cancer progression in�vitro and in�vivo

Lin

et al. 2020

Int J Oncol

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“…Although some SNPs have been identified in IGF1R, the high expression of IGF1R and its mRNA without any mutations has been frequently discovered in transformed cells [56,57]. By looking at its functions exclusively in cancers, IGF1R activation works coordinately with several downstream pathways including PI3K/AKT, Ras/Raf/MAPK and STAT to induce oncogenic transformation, cellular outgrowth, apoptotic resistance, migration, metastasis and angiogenesis [58]. At least three ligands have been reported to bind and stimulate IGF1R.…”

Section: Ubqlns and Membrane Receptor Proteinsmentioning

confidence: 99%

Ubiquilin Networking in Cancers

Jantrapirom

Piccolo

Pruksakorn

et al. 2020

Cancers

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Ubiquilins or UBQLNs, members of the ubiquitin-like and ubiquitin-associated domain (UBL-UBA) protein family, serve as adaptors to coordinate the degradation of specific substrates via both proteasome and autophagy pathways. The UBQLN substrates reveal great diversity and impact a wide range of cellular functions. For decades, researchers have been attempting to uncover a puzzle and understand the role of UBQLNs in human cancers, particularly in the modulation of oncogene’s stability and nucleotide excision repair. In this review, we summarize the UBQLNs’ genetic variants that are associated with the most common cancers and also discuss their reliability as a prognostic marker. Moreover, we provide an overview of the UBQLNs networks that are relevant to cancers in different ways, including cell cycle, apoptosis, epithelial-mesenchymal transition, DNA repairs and miRNAs. Finally, we include a future prospective on novel ubiquilin-based cancer therapies.

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“…In triple-negative breast cancer, stromal cancer-associated fibroblasts were identified as the source of IGF-1 and CXCL12, which were shown to prime cells to home to the CXCL12-and IGF-1-rich bone microenvironment, in a process dependent on CXCR4 and IGF-1R expression by cancer cells (55). IGF-1 also enhances homing of myeloma cells to bone marrow, and acts as a chemo-attractant that increases adherence to the extracellular matrix via activation of beta integrin and PI3K/AKT (56). IGF-1R upregulation was shown to promote adherence of neuroblastoma cells to human bone marrow endothelial cells, and transendothelial migration was decreased by IGF-1R inhibition (57).…”

Section: The Role Of the Igf Axis In Bone Metastasesmentioning

confidence: 99%

Bad to the Bone: The Role of the Insulin-Like Growth Factor Axis in Osseous Metastasis

Rieunier

Macaulay

et al. 2019

Clinical Cancer Research

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Bone metastases are a frequent complication of cancer that are associated with considerable morbidity. Current treatments may temporarily palliate the symptoms of bone metastases but often fail to delay their progression. Bones provide a permissive environment because they are characterized by dynamic turnover, secreting factors required for bone maintenance but also stimulating the establishment and growth of metastases. Insulin-like growth factors (IGF) are the most abundant growth factors in bone and are required for normal skeletal development and function. Via activation of the IGF-1 receptors (IGF-1R) and variant insulin receptors, IGFs promote cancer progression, aggressiveness, and treatment resistance. Of specific relevance to bone biology, IGFs contribute to the homing, dormancy, colonization, and expansion of bone metastases. Furthermore, preclinical evidence suggests that tumor cells can be primed to metastasize to bone by a high IGF-1 environment in the primary tumor, suggesting that bone metastases may reflect IGF dependency. Therapeutic targeting of the IGF axis may therefore provide an effective method for treating bone metastases. Indeed, anti-IGF-1R antibodies, IGF-1R tyrosine kinase inhibitors, and anti-IGF-1/2 antibodies have demonstrated antitumor activity in preclinical models of prostate and breast cancer metastases, either alone or in combination with other agents. Several studies suggest that such treatments can inhibit bone metastases without affecting growth of the primary tumor. Although previous trials of anti-IGF-1R drugs have generated negative results in unselected patients, these considerations suggest that future clinical trials of IGF-targeted agents may be warranted in patients with bone metastases.

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Type I insulin-like growth factor receptor signaling in hematological malignancies

Cited by 42 publications

References 293 publications

Knockdown of GSG2 inhibits prostate cancer progression in�vitro and in�vivo

Knockdown of GSG2 inhibits prostate cancer progression in�vitro and in�vivo

Ubiquilin Networking in Cancers

Bad to the Bone: The Role of the Insulin-Like Growth Factor Axis in Osseous Metastasis

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