Notch pathway promotes ovarian cancer growth and migration via CXCR4/SDF1α chemokine system

Chiaramonte, Raffaella; Colombo, M.; Bulfamante, Gaetano; Falleni, Monica; Tosi, Delfina; Garavelli, S.; Simone, D. De; Vigolo, Emilia; Todoerti, Katia; Neri, Antonino; Platonova, N.

doi:10.1016/j.biocel.2015.07.015

Cited by 44 publications

(39 citation statements)

References 39 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…CXCL12‐CXCR4 axis is strongly linked to intraperitoneal dissemination of ovarian cancer . Our group and others have corroborated that the CXCL12‐CXCR4 chemokine axis plays a critical role in ovarian cancer metastasis through mediating a variety of cellular functions such as cell proliferation, migration, invasion, and adhesion . As one of the major chemokine receptors, CXCR4 has been demonstrated to be aberrantly expressed in a variety of human cancers, including ovarian cancer, but its expression is low or absent in many normal tissues, including ovary .…”

Section: Introductionsupporting

confidence: 63%

CXCR7 is not obligatory for CXCL12‐CXCR4‐induced epithelial‐mesenchymal transition in human ovarian cancer

Zheng

Liu

Chen

et al. 2018

Molecular Carcinogenesis

View full text Add to dashboard Cite

Although the CXCL12‐CXCR4/CXCR7 chemokine axis is demonstrated to play an integral role in tumor progression, the controversy exists and the role of CXCL12‐CXCR4/CXCR7 signaling axis in epithelial‐mesenchymal transition (EMT) of human ovarian cancer has not been explored. Here, we showed that in ovarian cancer CXCL12 induced EMT phenotypes including the spindle‐like cell morphology, podia and stress fiber formation, a decrease in E‐cadherin expression, and increases in mesenchymal N‐cadherin and vimentin expressions. These effects of CXCL12 could be antagonized by the CXCR4 antagonist AMD3100, but not by the anti‐CXCR7 antibody. The expressions of the EMT markers were significantly down‐regulated by the CXCR4 siRNA, and up‐regulated by the pcDNA3.1/CXCR4 plasmid, whereas not affected by the CXCR7 siRNA. Furthermore, intraperitoneal administration of AMD3100 inhibited tumor dissemination and growth in the nude mice inoculated with ovarian IGROV‐1 cells with a concomitant reduction in EMT marker expressions. Collectively, these data suggest that CXCR4, rather than CXCR7, plays a key role in CXCL12‐activated EMT phenotypes, and targeting the CXCL12‐CXCR4 chemokine axis represents a potential therapeutic strategy to prevent ovarian cancer progression.

show abstract

Section: Introductionsupporting

confidence: 63%

CXCR7 is not obligatory for CXCL12‐CXCR4‐induced epithelial‐mesenchymal transition in human ovarian cancer

Zheng

Liu

Chen

et al. 2018

Molecular Carcinogenesis

View full text Add to dashboard Cite

show abstract

“…In lung cancer cells, Zhang S et al demonstrated the inhibition of CK2α down-regulated Notch1 signaling, which is usually involved in cancer cell proliferation [41]. In ovarian cancer, Chiaramonte R et al found that the Notch pathway also can promote cell growth via the CXCR4/SDF1α chemokine system [42]. …”

Section: Discussionmentioning

confidence: 99%

Increased expression of protein kinase CK2α correlates with poor patient prognosis in epithelial ovarian cancer

Wang

He³

et al. 2017

PLoS ONE

View full text Add to dashboard Cite

Epithelial ovarian cancer (EOC) is one of the deadly gynecological malignancies. The function of protein kinase CK2α (CK2α) in EOC is still unknown. Our study aimed to investigate the relationship between the protein expression of CK2α and the tumor progression, the prognosis of human EOC. In this study, we analyzed the expression levels of CK2α through Western blot, using EOC cell lines like A2780, HO8910, COV644, OVCAR3, SKOV3, and the primary normal ovarian surface epithelial (NOSE) cells. Furthermore, OVCAR3 and SKOV3 EOC cells were employed as a cellular model to study the role of CK2α on cell growth, migration, invasion, apoptosis, and cell cycle distribution. In addition, we investigated CK2α protein expression in tumor tissues from patients with EOC by immunohistochemistry and analyzed the association between CK2α expression and clinicopathologic parameters and prognosis of EOC patients. And we found that compared with NOSE cells, CK2α protein expression was increased in A2780, HO8910, OVCAR3, and SKOV3 ovarian cancer cell lines. Decreased CK2α expression suppressed OVCAR3 and SKOV3 cell growth and induced more apoptosis. CK2α knockdown using specific siRNAs inhibited migration and invasion ability of OVCAR3 and SKOV3 cells. In addition, high CK2α protein expression was found in 68.4% (80/117) of EOC patients. Increased CK2α expression of was significantly correlated with FIGO staging and peritoneal cytology. Patients with higher CK2α expression had a significantly poorer overall survival compared with those with lower CK2α expression. Multi-variate Cox regression analysis proved that increased CK2α expression was an independent prognostic marker for EOC. Taken together, our data displayed that CK2α may play a role in tumor aggressive behavior of EOC and could be used as a marker for predicting prognosis of EOC patient. High CK2α expression might predict poor patient survival.

show abstract

“…Furthermore, some studies supplement chemotactic factor in culture medium to enhance cell invasion and migration ability. It has been illustrated that Notch signaling regulated ovarian cancer cell migration by increasing SDF1 expression (5).…”

Section: Discussionmentioning

confidence: 99%

“…Dysregulation of Notch receptors, ligands, or target genes is noted in various cancer cells (1,2). Notch signaling inhibition has been demonstrated to attenuate cancer cell proliferation/cell cycle progression, to decrease cancer cell viability, and to increase cell apoptosis in various types of cancer (1,(3)(4)(5)(6). Furthermore, Notch signaling inhibition is proposed as an alternative adjuvant therapy for radiotherapy and chemotherapy (7,8).…”

Section: Introductionmentioning

confidence: 99%

Expression and influence of Notch signaling in oral squamous cell carcinoma

Osathanon

Nowwarote

Pavasant

2016

Journal of Oral Science

View full text Add to dashboard Cite

Notch pathway promotes ovarian cancer growth and migration via CXCR4/SDF1α chemokine system

Cited by 44 publications

References 39 publications

CXCR7 is not obligatory for CXCL12‐CXCR4‐induced epithelial‐mesenchymal transition in human ovarian cancer

CXCR7 is not obligatory for CXCL12‐CXCR4‐induced epithelial‐mesenchymal transition in human ovarian cancer

Increased expression of protein kinase CK2α correlates with poor patient prognosis in epithelial ovarian cancer

Expression and influence of Notch signaling in oral squamous cell carcinoma

Contact Info

Product

Resources

About