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Review
. 2019 Dec 6;12(1):120.
doi: 10.1186/s13048-019-0588-z.

Ovarian cancer stem cells and targeted therapy

Vahideh Keyvani  1   2 , Moein Farshchian  3 , Seyed-Alireza Esmaeili  4   5 , Hadi Yari  6 , Meysam Moghbeli  2 , Seyed-Reza Kazemi Nezhad  7 , Mohammad Reza Abbaszadegan  8
Affiliations
Review

Ovarian cancer stem cells and targeted therapy (V体育安卓版)

Vahideh Keyvani et al. J Ovarian Res. .

Abstract

Background: Ovarian cancer has the highest ratio of mortality among gynecologic malignancies. Chemotherapy is one of the most common treatment options for ovarian cancer. However, tumor relapse in patients with advanced tumor stage is still a therapeutic challenge for its clinical management. VSports手机版.

Main body: Therefore, it is required to clarify the molecular biology and mechanisms which are involved in chemo resistance to improve the survival rate of ovarian cancer patients. Cancer stem cells (CSCs) are a sub population of tumor cells which are related to drug resistance and tumor relapse V体育安卓版. .

Conclusion: In the present review, we summarized the recent findings about the role of CSCs in tumor relapse and drug resistance among ovarian cancer patients. Moreover, we focused on the targeted and combinational therapeutic methods against the ovarian CSCs. V体育ios版.

Keywords: Cancer stem cell; Detection; Drug resistance; Isolation; Ovarian cancer VSports最新版本. .

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Conflict of interest statement (VSports手机版)

The authors declare that they have no competing interests.

Figures

Fig. 1
Fig. 1
Schematic overview of the WNT signaling pathway. Wnt binds to (triggers) the receptor. Axin is removed from the “destruction complex.” β-catenin transfers into the nucleus, binds to a transcription factor on DNA, and stimulates transcription of a protein. Binding of Wnt to the receptors Frizzled (Fz) and LRP6 primes to inhibition of β-catenin degradation. β-catenin in turn interrelates with members of the TCF/Lef-1 family of transcription factors to co-activate target gene transcription
Fig. 2
Fig. 2
Schematic overview of the hedgehog signaling pathway and some inhibitors of the pathway in preclinical and clinical revisions. a In the absence of HH ligands, PTCH inhibits the role of SMO, and GLI proteins are changed by proteosomes to the transcriptional repressor form (GLIR). b Interaction of HH ligands with PTCH unrepresses SMO and creates activated GLI factors (GLIA) which encourage transcription of downstream HH genes. The bound of HH/PTHC complex develops adopted in the endosome and degraded
Fig. 3
Fig. 3
Schematic overview of the Notch signaling pathway. Ligands of the Jagged and Delta-like families interrelate with Notch family receptors on an adjacent cell. The Notch receptor exists at the cell surface as a proteolytically cleaved heterodimer containing of a large ectodomain and a membrane-tethered intracellular domain. The receptor-ligand interaction makes two additional proteolytic cleavages that free the Notch intracellular domain (NICD) from the cell membrane. The NICD moves to the nucleus, where it procedures a complex with the RBPJ protein, dislocating a histone deacetylase (HDAc)-co-repressor (CoR) complex from the RBPJ protein. Components of an activation complex, such as MAML1 and histone acetyltransferases (HAc), are engaged to the NICD-RBPJ complex, leading to the transcriptional activation of Notch target genes
See this image and copyright information in PMC

VSports最新版本 - References

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