Sonic hedgehog stimulates glycolysis and proliferation of breast cancer cells: Modulation of PFKFB3 activation

Lyu, Pengwei; Gu, Yuanting; Li, Lin; Li, Jingruo; Wang, Yan; Zhang, Linfeng; Fu, Chao; Cao, Zhiyun

doi:10.1016/j.bbrc.2015.07.052

Cited by 34 publications

(30 citation statements)

References 28 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…This may indicate greater activation of the Shh signaling pathway leading to increased cell proliferation. The expression pattern of this protein in syndromic and sporadic OKCs is similar to that seen in breast tumors, which also showed more prominent cytoplasmic Shh expression when compared to normal tissues [20]. Shh, Ptch, Smo, and Gli1 expression in sporadic and syndromic OKCs were all positive in the epithelial layers [21].…”

Section: Discussionsupporting

confidence: 58%

Immunohistochemical evaluation of Sonic Hedgehog signaling pathway proteins (Shh, Ptch1, Ptch2, Smo, Gli1, Gli2, and Gli3) in sporadic and syndromic odontogenic keratocysts

et al. 2018

View full text Add to dashboard Cite

Our findings suggest that the expression patterns of important Shh pathway proteins can represent valuable markers for early diagnosis of NBCCS-associated OKCs, as the major criterion for the diagnosis of NBCCS is currently based on the late appearance of basal cellular carcinomas. Thus, standardizing a new diagnostic tool for diagnosis of NBCCS could be of great importance in the identification of therapeutic targets. We therefore suggest, as based on our findings, that OKCs showing high expression of Shh, Smo, and Gli1 are potentially associated with NBCCS.

show abstract

Section: Discussionsupporting

confidence: 58%

Immunohistochemical evaluation of Sonic Hedgehog signaling pathway proteins (Shh, Ptch1, Ptch2, Smo, Gli1, Gli2, and Gli3) in sporadic and syndromic odontogenic keratocysts

et al. 2018

View full text Add to dashboard Cite

show abstract

“…However, the higher proliferative activity observed in IL30 conditioned versus control tumors proves that the multiple signaling pathways triggered by the cytokine results, as a whole, in tumor growth and progression. In addition, at least in the triple-negative tumor, IL30 substantially upregulates SHH, which accelerates MDA-MB-231 cell proliferation (42) and is fundamental in the maintenance of a putative cancer stem cell compartment along with MYC, which is also upregulated by IL30 (43,44). Moreover, IL30 downmodulates a set of critical tumor suppressors such as PTEN (18), RARB (19), RASSF1 (20), SLIT2 (21), and particularly TP73 (22), which lead to alterations in the cell-cycle regulation and a defective apoptotic response.…”

Section: Discussionmentioning

confidence: 99%

Interleukin-30 Promotes Breast Cancer Growth and Progression

et al. 2016

View full text Add to dashboard Cite

The inflammatory tissue microenvironment that promotes the development of breast cancer is not fully understood. Here we report a role for elevated IL30 in supporting the breast cancer cell viability and invasive migration. IL30 was absent in normal mammary ducts, ductules, and acini of histologically normal breast and scanty in the few stromal infiltrating leukocytes. In contrast, IL30 was expressed frequently in breast cancer specimens where it was associated with triple-negative and HER2 þ molecular subtypes. In stromal leukocytes found in primary tumors or tumor-draining lymph nodes, which included mainly CD14 þ monocytes, CD68 þ macrophages, and

show abstract

“…Furthermore, the AMPK-dependent phosphorylation of PFKFB3 substitutes oxidative respiration by glycolysis, which causes inhibition of cell death and of antitumor efficiency of the microtubule toxin in breast cancer cells (91). Sonic hedgehog phosphorylates PFKFB3 to promote glycolysis and proliferation of breast cancer cells, which is mediated by smoothened and p38/MK2 (92). In addition, the 6-phosphofructo-2-kinase/fructose-2,6-bisphosphatase 4 (PFKFB4) in breast cancer cells can phosphorylate the oncogenic steroid receptor coactivator-3, which rapidly increases its transcriptional activity and promotes the glucose flux switch towards purine synthesis (93).…”

Section: Ppp In Malignant Tumorsmentioning

confidence: 99%

Crucial role of the pentose phosphate pathway in malignant tumors (Review)

2019

View full text Add to dashboard Cite

Interest in cancer metabolism has increased in recent years. The pentose phosphate pathway (PPP) is a major glucose catabolism pathway that directs glucose flux to its oxidative branch and leads to the production of a reduced form of nicotinamide adenine dinucleotide phosphate and nucleic acid. The PPP serves a vital role in regulating cancer cell growth and involves many enzymes. The aim of the present review was to describe the recent discoveries associated with the deregulatory mechanisms of the PPP and glycolysis in malignant tumors, particularly in hepatocellular carcinoma, breast and lung cancer. Contents 1. Introduction 2. Glucose in the PPP 3. Glucose breakdown through glycolysis in the PPP 4. PPP in malignant tumors 5. Perspectives

show abstract

Sonic hedgehog stimulates glycolysis and proliferation of breast cancer cells: Modulation of PFKFB3 activation

Cited by 34 publications

References 28 publications

Immunohistochemical evaluation of Sonic Hedgehog signaling pathway proteins (Shh, Ptch1, Ptch2, Smo, Gli1, Gli2, and Gli3) in sporadic and syndromic odontogenic keratocysts

Immunohistochemical evaluation of Sonic Hedgehog signaling pathway proteins (Shh, Ptch1, Ptch2, Smo, Gli1, Gli2, and Gli3) in sporadic and syndromic odontogenic keratocysts

Interleukin-30 Promotes Breast Cancer Growth and Progression

Crucial role of the pentose phosphate pathway in malignant tumors (Review)

Contact Info

Product

Resources

About