Hypoxic control of metastasis

In the paper

“Clinically, hypoxia is associated with HIF activation, metastasis, and resistance to chemotherapy and radiotherapy, as well as poor patient survival”

What the sources say

• Not checked yetcites [4] Rankin EB Giaccia AJ Cell Death Differ 2008 15 678 685 18259193 PMC3050610 source
• ?Not matched

  Couldn’t be matched to a paper in Crossref, so it can’t be checked.

  cites [5] Schindl M Clin. Cancer Res 2002 8 1831 1837 12060624
• Not checked yetcites [6] Yamamoto Y Breast Cancer Res. Treat 2008 110 465 475 17805961 source

In the paper

“Clinically, HIF-1 and HIF-2 are highly expressed in primary tumors and metastases.”

• Also stated in: § Hypoxic signaling · hedged

  “increased HIF expression is often linked with increased patient mortality in a variety of human cancers”

What the sources say

• Not checked yetcites [41] Semenza GL Oncogene 2010 29 625 634 19946328 PMC2969168 source

In the paper

“It has been estimated that 50 to 60% of solid tumors contain regions of hypoxia and/or anoxia”

What the sources say

• Not checked yetcites [2] Vaupel P Mayer A Cancer Metastasis Rev 2007 26 225 239 17440684 source

In the paper

“In tumor cells, mutations in the genes encoding succinate dehydrogenase (SDH) or fumarate hydratase (FH) cause the accumulation of cytosolic succinate or fumarate; this inhibits the activity of prolyl hydroxylases and leads to HIF stabilization under normoxic conditions”

What the sources say

• Not checked yetcites [22] Kaelin WG Jr. Cold Spring Harb. Symp. Quant. Biol 2011 76 335 345 22089927 PMC4197849 source

In the paper

“As a result, EGLN 1–3 activity and HIF-α stability are affected by iron availability and can be inhibited by Krebs cycle intermediates, including succinate and fumarate, which compete with 2-oxoglutarate”

What the sources say

• Not checked yetcites [18] Pan Y Mol. Cell. Biol 2007 27 912 925 17101781 PMC1800695 source
• Not checked yetcites [19] Nandal A Cell Metab 2011 14 647 657 22055506 PMC3361910 source
• Not checked yetcites [20] Jones DT Trowbridge IS Harris AL Cancer Res 2006 66 2749 2756 16510596 source
• Not checked yetcites [21] Majmundar AJ Wong WJ Simon MC Mol. Cell 2010 40 294 309 20965423 PMC3143508 source
• Not checked yetcites [22] Kaelin WG Jr. Cold Spring Harb. Symp. Quant. Biol 2011 76 335 345 22089927 PMC4197849 source

In the paper

“these factors allow cells to survive and adapt to low oxygen tensions, as well as confer changes in both and host that promote metastasis”

In the paper

“Under hypoxic conditions, PHD activity is inhibited, resulting in HIF-α stabilization and translocation to the nucleus.”

In the paper

“WSB1 expression in tumor cells leads to HIF stabilization under normoxic and hypoxic conditions and correlates with metastasis in cancer patients”

What the sources say

• Not checked yetcites [27] Kim JJ Genes Dev 2015 29 2244 2257 26545811 PMC4647558 source

In the paper

“Although genetic inactivation of VHL is thought to be an early event in the pathogenesis of ccRCC”

In the paper

“Genetic mutations or epigenetic inactivation of VHL causes VHL disease, which is associated with constitutive activation of HIF-1 and HIF-2 and the development of highly vascularized tumors”

In the paper

“Both HIF-α mRNA transcription and translation are regulated by TORC1 activity”

What the sources say

• Not checked yetcites [22] Kaelin WG Jr. Cold Spring Harb. Symp. Quant. Biol 2011 76 335 345 22089927 PMC4197849 source

In the paper

“Renal cell carcinoma is a major cause of morbidity in VHL patients, owing to the ability of these tumors to metastasize to other tissue sites”

What the sources say

• Not checked yetcites [24] Lonser RR Lancet 2003 361 2059 2067 12814730

In the paper

“UCHL1 is associated with HIF-1 and distant metastasis in cancer patients”

What the sources say

• Not checked yetcites [35] Goto Y Nat. Commun 2015 6 6153 25615526 PMC4317501 source

In the paper

“HIF-1 mRNA translation can be enhanced under normoxic and hypoxic conditions through the binding of YB-1, an RNA and DNA binding protein; this leads to increased HIF-1 protein and prometastatic activity in sarcoma cells”

What the sources say

• Not checked yetcites [34] El-Naggar AM Cancer Cell 2015 27 682 697 25965573

In the paper

“respiratory hyperoxia was associated with a decrease in intratumoral hypoxia and an immunopermissive tumor microenvironment characterized by abundant CD8+ T cell infiltration and decreased regulatory T cell infiltration”

What the sources say

• Not checked yetcites [50] Hatfield SM Sci. Transl. Med 2015 7 277ra30 PMC4641038 25739764 source

In the paper

“In preclinical models, respiratory hyperoxia (60% O2) can promote tumor regression, reduce metastatic disease, and prolong animal survival”

What the sources say

• Not checked yetcites [50] Hatfield SM Sci. Transl. Med 2015 7 277ra30 PMC4641038 25739764 source

In the paper

“Once in the tumor microenvironment, Tregs promote immune tolerance and angiogenesis, which supports metastatic tumor growth”

What the sources say

• Not checked yetcites [60] Facciabene A Nature 2011 475 226 230 21753853 source

In the paper

“Hypoxic signaling in MDSCs and macrophages directly contributes to tumor progression by promoting an immunosuppressive phenotype and stimulating angiogenesis”

What the sources say

• Not checked yetcites [57] Palazon A Goldrath AW Nizet V Johnson RS Immunity 2014 41 518 528 25367569 PMC4346319 source
• Not checked yetcites [61] Corzo CA J. Exp. Med 2010 207 2439 2453 20876310 PMC2964584 source
• Not checked yetcites [62] Colegio OR Nature 2014 513 559 563 25043024 PMC4301845 source
• Not checked yetcites [63] Chaturvedi P Gilkes DM Takano N Semenza GL Proc. Natl. Acad. Sci. U.S.A 2014 111 E2120 E2129 24799675 PMC4034192 source

In the paper

“Hypoxic signaling can promote resistance to T cell–mediated killing by increasing the expression of programmed death–ligand 1 (PD-L1) on tumor cells and myeloid-derived suppressor cells (MDSCs), and by enhancing CTLA-4 expression on CD8+ T cells”

What the sources say

• Not checked yetcites [57] Palazon A Goldrath AW Nizet V Johnson RS Immunity 2014 41 518 528 25367569 PMC4346319 source

In the paper

“Cell-cell adhesions are mediated primarily by cadherin proteins expressed at intercellular junctions”

What the sources say

• Not checked yetcites [65] Cavallaro U Christofori G Nat. Rev. Cancer 2004 4 118 132 14964308

In the paper

“Loss of AXL does not appear to have deleterious effects on embryonic development or normal adult tissue function in mice”

What the sources say

• Not checked yetcites [87] Lu Q Nature 1999 398 723 728 10227296 source
• Not checked yetcites [88] Angelillo-Scherrer A Nat. Med 2001 7 215 221 11175853 source

In the paper

“biological inhibitors of AXL, such as soluble AXL decoy receptors, are specific and are not associated with normal tissue or hematologic toxicities in mice”

What the sources say

• Not checked yetcites [82] Rankin EB Cancer Res 2010 70 7570 7579 20858715 PMC3408227
• Not checked yetcites [89] Kariolis MS Nat. Chem. Biol 2014 10 977 983 25242553 PMC4372605

In the paper

“Given that LOX also promotes tumor cell proliferation, invasion, and angiogenesis, LOX is an attractive therapeutic target for cancer therapy (97).”

What the sources say

• Not checked yetcites [97] Cox TR Gartland A Erler JT Cancer Res 2016 76 188 192 26732355

In the paper

“IL-6 secretion by the tumor activates signal transducer and activator of transcription 3 (STAT3) signaling in LECs localized within the lymph node and lung to promote (i) CCL5-mediated recruitment of CCR5-positive breast cancer cells into the lymphatic system and (ii) VEGF-mediated lung vascular permeability and lymph node angiogenesis (98).”

What the sources say

• Not checked yetcites [98] Lee E Nat. Commun 2014 5 4715 25178650 PMC4351998 source

In the paper

“Moreover, tumor-derived exosomes preferentially localize to sites of metastasis, including liver, lung, and bone marrow, where they promote vascular permeability and increase BMDC recruitment (101–104).”

What the sources say

• Not checked yetcites [101] Peinado H Nat. Med 2012 18 883 891 22635005 PMC3645291 source
• Not checked yetcites [102] Costa-Silva B Nat. Cell Biol 2015 17 816 826 25985394 PMC5769922 source
• Not checked yetcites [103] Hoshino A Nature 2015 527 329 335 26524530 PMC4788391 source
• Not checked yetcites [104] Umezu T Blood 2014 124 3748 3757 25320245 PMC4263983 source

In the paper

“Because oxygen is an essential electron acceptor for oxidative metabolism, hepatocytes that perform glucose or fatty acid oxidation are located in the aerobic periportal zone, whereas oxygen-independent metabolic functions such as glucose uptake, glycolysis, and fatty acid synthesis are predominantly performed by perivenous hepatocytes (108).”

What the sources say

• Not checked yetcites [108] Jungermann K Semin. Liver Dis 1988 8 329 341 3062788

In the paper

“The partial pressure of oxygen in periportal blood is 60 to 65 mm Hg and in the perivenous blood it is 30 to 35 mm Hg (107).”

What the sources say

• Not checked yetcites [107] Jungermann K Kietzmann T Hepatology 2000 31 255 260 10655244

In the paper

“VEGF-A is a proangiogenic factor produced by tumor cells that stimulates the recruitment and proliferation of endothelial cells, as well as promoting pericyte proliferation and migration (113).”

What the sources say

• Not checked yetcites [113] Joyce JA Pollard JW Nat. Rev. Cancer 2009 9 239 252 19279573 PMC3251309 source

In the paper

“suggesting that hepatic hypoxia is a barrier for colon cancer cells early in metastatic dissemination and that cells overcome this metabolic stress by generating ATP from phosphocreatine reserves (Fig. 3) (109).”

What the sources say

• Not checked yetcites [109] Loo JM Cell 2015 160 393 406 25601461 PMC4312495 source

In the paper

“VEGF-A is a well-established HIF target, and its expression is induced by HIF signaling in both primary tumors and metastases (114).”

What the sources say

• Not checked yetcites [114] Maxwell PH Proc. Natl. Acad. Sci. U.S.A 1997 94 8104 8109 9223322 PMC21564 source

In the paper

“Recent work has identified the receptor tyrosine kinase, AXL, as a critical mediator of HIF-dependent invasion and metastasis, as well as a potential therapeutic target for the prevention and treatment of metastatic disease.”

In the paper

“In summary, recent studies have begun to highlight the diverse mechanisms by which hypoxia and HIF-dependent signaling promote metastatic tumor progression.”