Dickkopf homolog 3 (<i>DKK3</i>): A candidate for detection and treatment of cancers?

Hamzehzadeh, Leila; Caraglia, Michele; Atkin, Stephen L.; Sahebkar, Amirhossein

doi:10.1002/jcp.26313

Cited by 24 publications

(21 citation statements)

References 80 publications

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“…In our study, LINC00261 is expressed at a low level in prostate cancer, and LINC00261 negatively correlates with prostate cancer progression. Increasing studies have demonstrated that the aberrant expression of DKK3 is associated with the proliferation and tumor development and it is already considered to be a biomarker and therapeutic target in many cancers [7].…”

Section: Discussionmentioning

confidence: 99%

“…As a divergent member of the Dickkopf (DKK) family, the Dickkopf-related protein 3 (DKK3) is a tumor suppressor involved in slowing down the progressions of many types of cancer. For example, DKK3 is expressed at a low level in endometrial cancer, indicating that DKK3 can also be used as a new biomarker in endometrial cancer [7]. In addition, a recent study has shown that induction of DKK3 can inhibit prostate cancer development [8].…”

Section: Introductionmentioning

confidence: 99%

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Long noncoding RNA LINC00261 suppresses prostate cancer tumorigenesis through upregulation of GATA6-mediated DKK3

Wei

2020

Cancer Cell Int

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Background Prostate cancer is one of the leading causes of cancer death in males. Recent studies have reported aberrant expression of lncRNAs in prostate cancer. This study explores the role of LINC00261 in prostate cancer progression. Methods The differentially expressed genes, transcription factors, and lncRNAs related to prostate cancer were predicted by bioinformatics analysis. Prostate cancer tissue samples and cell lines were collected for the determination of the expression of LINC00261 by reverse transcription quantitative polymerase chain reaction. The binding capacity of LINC00261 to the transcription factor GATA6 was detected by RIP, and GATA6 binding to the DKK3 promoter region was assessed by ChIP. In addition, luciferase reporter system was used to verify whether LINC00261 was present at the DKK3 promoter. After gain- and loss-of function approaches, the effect of LINC00261 on prostate cancer in vitro and in vivo was assessed by the determination of cell proliferation, invasion and migration as well as angiogenesis. Results LINC00261, GATA6, and DKK3 were poorly expressed in prostate cancer. LINC00261 could inhibit transcriptional expression of DKK3 by recruiting GATA6. Overexpression of LINC00261 inhibited prostate cancer cells proliferation, migration, and invasion as well as angiogenesis, which could be reversed by silencing DKK3. Furthermore, LINC00261 could also suppress the tumorigenicity of cancer cells in vivo. Conclusions Our study demonstrates the inhibitory role of LINC00261 in prostate cancer progression, providing a novel biomarker for early detection of prostate cancer.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Long noncoding RNA LINC00261 suppresses prostate cancer tumorigenesis through upregulation of GATA6-mediated DKK3

Wei

2020

Cancer Cell Int

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“…DKK3, found to be increased at the gene and protein level in FCA, is considered to be a tumor suppressor involved in several cancers [ 57 ] and, most interestingly, described as required for maintaining the integrity of secretory vesicles in mouse adrenal glands [ 58 ]. Further studies with regard to this marker might reveal its role in modulating both hormone production and tumor growth restriction in corticotroph adenomas.…”

Section: Discussionmentioning

confidence: 99%

Distinct Pattern of Endoplasmic Reticulum Protein Processing and Extracellular Matrix Proteins in Functioning and Silent Corticotroph Pituitary Adenomas

Eieland

Normann

Sundaram

et al. 2020

Cancers

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Functioning (FCA) and silent corticotroph (SCA) pituitary adenomas act differently from a clinical perspective, despite both subtypes showing positive TBX19 (TPIT) and/or adrenocorticotropic hormone (ACTH) staining by immunohistochemistry. They are challenging to treat, the former due to functional ACTH production and consequently hypercortisolemia, and the latter due to invasive and recurrent behavior. Moreover, the molecular mechanisms behind their distinct behavior are not clear. We investigated global transcriptome and proteome changes in order to identify signaling pathways that can explain FCA and SCA differences (e.g., hormone production vs. aggressive growth). In the transcriptomic study, cluster analyses of differentially expressed genes revealed two distinct groups in accordance with clinical and histological classification. However, in the proteomic study, a greater degree of heterogeneity within the SCA group was found. Genes and proteins related to protein synthesis and vesicular transport were expressed by both adenoma groups, although different types and a distinct pattern of collagen/extracellular matrix proteins were presented by each group. Moreover, several genes related to endoplasmic reticulum protein processing were overexpressed in the FCA group. Together, our findings shed light on the different repertoires of activated signaling pathways in corticotroph adenomas, namely, the increased protein processing capacity of FCA and a specific pattern of adhesion molecules that may play a role in the aggressiveness of SCA.

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“…In gastric cancer, DKK3 was shown to attenuate CD133-induced NK-cell activation by inhibiting the Erk pathway and immunological synapse formation (27). DKK3 was also found to act as a biomarker and a therapeutic target by modulating Wnt signaling in several types of human cancer (28). However, the role of DKK3 in TC remains understudied.…”

Section: Discussionmentioning

confidence: 99%

MicroRNA‑3690 promotes cell proliferation and cell cycle progression by altering DKK3 expression in human thyroid cancer

et al. 2020

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An increasing amount of evidence has demonstrated the importance of microRNAs (miRNAs/miRs) in the tumorigenesis of malignant types of cancer, and data retrieved from The Cancer Genome Atlas database revealed that miR-3690 was upregulated in thyroid cancer (TC). The present study focused on the biological function and mechanism of miR-3690 in TC, demonstrating that miR-3690 expression was significantly elevated in TC cells and clinical tissues. Functional studies indicated that miR-3690 acted as an oncogene in TC by promoting cell proliferation, colony formation and cell cycle progression in association with the increased expression of cyclin E and c-myc. Mechanistically, prediction software indicated that Dickkopf-related protein 3 (DKK3) was a target of miR-3690, which was confirmed by the results of luciferase reporter assays and western blotting. DKK3 silencing abrogated the functions of miR-3690-in on TC cell proliferation. Collectively, the findings of the present study demonstrated that miR-3690 promoted TC cell proliferation and indicated miR-3690 as a potential biomarker and therapeutic target for TC.

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Dickkopf homolog 3 (DKK3): A candidate for detection and treatment of cancers?

Cited by 24 publications

References 80 publications

Long noncoding RNA LINC00261 suppresses prostate cancer tumorigenesis through upregulation of GATA6-mediated DKK3

Long noncoding RNA LINC00261 suppresses prostate cancer tumorigenesis through upregulation of GATA6-mediated DKK3

Distinct Pattern of Endoplasmic Reticulum Protein Processing and Extracellular Matrix Proteins in Functioning and Silent Corticotroph Pituitary Adenomas

MicroRNA‑3690 promotes cell proliferation and cell cycle progression by altering DKK3 expression in human thyroid cancer

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