Sonic hedgehog signaling regulates Bcr-Abl expression in human chronic myeloid leukemia cells

Liao, Hui-Fen; Su, Yu Chieh; Zheng, Zhiyu; Cai, Chang; Hou, Ming-Hung; Chao, K.S. Clifford; Chen, Yu-Jen

doi:10.1016/j.biopha.2011.12.008

Cited by 29 publications

(24 citation statements)

References 19 publications

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“…Regulation of CSC proliferation in various human tumors including glioblastoma, breast cancer, pancreatic adenocarcinoma, MM and CML is through Hh signaling [97,233-241]. Use of the SMO antagonist cyclopamine or the Hh ligand neutralizing antibody 5E1 induced terminal differentiation and loss of clonogenic growth in gastric CSCs from primary tumors [242,243].…”

Section: Molecular Pathways Regulating Tumor Proliferationmentioning

confidence: 99%

Sustained proliferation in cancer: Mechanisms and novel therapeutic targets

Feitelson

Arzumanyan

Kulathinal

et al. 2015

Seminars in Cancer Biology

503

357

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Proliferation is an important part of cancer development and progression. This is manifest by altered expression and/or activity of cell cycle related proteins. Constitutive activation of many signal transduction pathways also stimulates cell growth. Early steps in tumor development are associated with a fibrogenic response and the development of a hypoxic environment which favors the survival and proliferation of cancer stem cells. Part of the survival strategy of cancer stem cells may manifested by alterations in cell metabolism. Once tumors appear, growth and metastasis may be supported by overproduction of appropriate hormones (in hormonally dependent cancers), by promoting angiogenesis, by undergoing epithelial to mesenchymal transition, by triggering autophagy, and by taking cues from surrounding stromal cells. A number of natural compounds (e.g., curcumin, resveratrol, indole-3-carbinol, brassinin, sulforaphane, epigallocatechin-3-gallate, genistein, ellagitannins, lycopene and quercetin) have been found to inhibit one or more pathways that contribute to proliferation (e.g., hypoxia inducible factor 1, nuclear factor kappa B, phosphoinositide 3 kinase/Akt, insulin-like growth factor receptor 1, Wnt, cell cycle associated proteins, as well as androgen and estrogen receptor signaling). This data, in combination with bioinformatics analyses, will be very important for identifying signaling pathways and molecular targets that may provide early diagnostic markers and/or critical targets for the development of new drugs or drug combinations that block tumor formation and progression.

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Section: Molecular Pathways Regulating Tumor Proliferationmentioning

confidence: 99%

Sustained proliferation in cancer: Mechanisms and novel therapeutic targets

Feitelson

Arzumanyan

Kulathinal

et al. 2015

Seminars in Cancer Biology

503

357

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“…A significant decrease in extracellular level of vascular endothelial growth factor (VEGF) has been associated with apoptosis following Res treatment in breast cancer cells (Garvin et al, 2006). Recent studies also suggest that Res inhibits SHH signaling in human chronic and acute myeloid leukemic (CML and AML) cells indicating that Res could be used as a potent agent for the treatment of some aggressive cancer types (Liao et al, 2012;Su et al, 2014). However, Res metabolites have very short half-life and are prone to rapid renal clearance.…”

Section: Introductionmentioning

confidence: 98%

Resveratrol and curcumin synergistically induces apoptosis in cigarette smoke condensate transformed breast epithelial cells through a p21Waf1/Cip1 mediated inhibition of Hh-Gli signaling

Mohapatra

Satapathy

Siddharth

et al. 2015

The International Journal of Biochemistry & Cell Biology

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“…The inhibition of sonic hedgehog (Shh) signaling downregulates the expression of the ATP-binding cassette transporter multidrug resistant (MDR) proteins, and thus may be a target for overcoming drug resistance and increasing the likelihood of response to chemotherapy [12]. Our previous study demonstrated that Shh signaling molecules expressed in human chronic myeloid leukemia (CML) cells may regulate Bcr-Abl activation [13]. In addition, a research indicated that thalidomide reduces vascular endothelial growth factor (VEGF) and interleukin (IL)-6 expression in the tumor microenvironment accounts, as well as attenuates Hh signaling activity in advanced prostate cancers [14].…”

Section: Introductionmentioning

confidence: 99%

Resveratrol Downregulates Interleukin-6-Stimulated Sonic Hedgehog Signaling in Human Acute Myeloid Leukemia

et al. 2013

Evidence-Based Complementary and Alternative Medicine

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IL-6 and sonic hedgehog (Shh) signaling molecules are considered to maintain the growth of cancer stem cells (CSCs). Resveratrol, an important integrant in traditional Chinese medicine, possesses certain antitumor effects. However, the mechanisms on regulating acute myeloid leukemia (AML) are unclear. This study first used human subjects to demonstrate that the plasma levels of IL-6 and IL-1β in AML patients were higher and lower, respectively, than healthy donors. The expression of Shh preproproteins, and C- and N-terminal Shh peptides increased in bone marrow and peripheral blood mononuclear cells isolated from AML patients, and the plasma N-Shh secretion was greater. To further clarify the effect of IL-6 and resveratrol in Shh signaling, human AML HL-60 cells were tested. IL-6 upregulated Shh and Gli-1 expression and was accompanied by an increase of cell viability. Resveratrol significantly decreased CSC-related Shh expression, Gli-1 nuclear translocation, and cell viability in IL-6-treated HL-60 cells and had synergistic effect with Shh inhibitor cyclopamine on inhibiting cell growth. Conclusions. IL-6 stimulated the growth of AML cells through Shh signaling, and this effect might be blocked by resveratrol. Further investigations of Shh as a prognostic marker and resveratrol as a therapeutic drug target to CSCs in AML are surely warranted.

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Sonic hedgehog signaling regulates Bcr-Abl expression in human chronic myeloid leukemia cells

Cited by 29 publications

References 19 publications

Sustained proliferation in cancer: Mechanisms and novel therapeutic targets

Sustained proliferation in cancer: Mechanisms and novel therapeutic targets

Resveratrol and curcumin synergistically induces apoptosis in cigarette smoke condensate transformed breast epithelial cells through a p21Waf1/Cip1 mediated inhibition of Hh-Gli signaling

Resveratrol Downregulates Interleukin-6-Stimulated Sonic Hedgehog Signaling in Human Acute Myeloid Leukemia

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