DRG2 supports the growth of primary tumors and metastases of melanoma by enhancing VEGF‐A expression

Yoon, Nal Ae; Jung, Seonghoon; Choi, Seong Hee; Ryu, Jin Hyun; Mani, Muralidharan; Lee, Unn Hwa; Vo, Mai-Tram; Jeon, Do Yong; Chung, Sung Min; Lee, Byung Ju; Koh, Young Wha; Park, Soon Eun; Shin, Yong Joon; Kang, Sang Soo; Cho, Wha Ja; Jeong, Hee; Park, Jeong Woo

doi:10.1111/febs.15125

Cited by 11 publications

(17 citation statements)

References 48 publications

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“…In the present study, the level of DRG2 expression differed in each prostate cancer cell line, being highest in LNCaP cells and lowest in DU145 cells. These results contradict those of a previously reported study on melanoma [ 20 ]. That study reported that VEGF-A expression was enhanced by DRG2 expression, thus promoting tumor growth and metastasis.…”

Section: Discussioncontrasting

confidence: 94%

“…In particular, DRG2 is reported to be involved in G2/M progression, and thus seems to play an important role in the cell response to genotoxic stress. The roles of DRG2 in T cell leukemia, cervical cancer, melanoma, lung cancer, and hepatocellular carcinoma have been reported, but there has been no such study on urological cancers [ 15 16 17 18 19 20 21 ]. Moreover, it is necessary to confirm the association between DRG2 and prostate cancer, which is treated with the chemotherapeutic agent docetaxel, an antimicrotubule agent.…”

Section: Introductionmentioning

confidence: 99%

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Developmentally regulated GTP-binding protein 2 levels in prostate cancer cell lines impact docetaxel-induced apoptosis

et al. 2021

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Purpose This study aimed to confirm the association between developmentally regulated GTP-binding protein 2 (DRG2) expression and docetaxel-induced apoptosis and to determine whether prostate cancer responses to docetaxel treatment differ with DRG2 expression. Materials and Methods PC3, DU145, and LNCaP prostate cancer cell lines were used. The MTT assay was used to determine cell viability. Western blotting analysis was performed using anti-DRG2 antibodies. Cells were transfected with 50 nmol DRG2 siRNA using an siRNA transfection reagent for DRG2 knockdown. The cell cycle was analyzed by using flow cytometry, and apoptosis was detected by using the Annexin V cell death assay. Results DRG2 expression differed in each prostate cancer cell line. Docetaxel reduced DRG2 expression in a dose-dependent manner. Upon DRG2 knockdown in prostate cancer cells, an increase in the sub-G1 phase was observed without a change in the G1 or G2/M phases. When 4 nM docetaxel was administered to DRG2 knockdown prostate cancer cell lines, an increase in the sub-G1 phase was observed without increasing the G2/M phase, which was similar to that in DU145 cells before DRG2 knockdown. In PC3 and DU145 cell lines, DRG2 knockdown increased docetaxel-induced Annexin V (+) apoptosis by 8.7 and 2.7 times, respectively. Conclusions In prostate cancer cells, DRG2 regulates G2/M arrest after docetaxel treatment. In prostate cancer cells with DRG2 knockdown, apoptosis increases without G2/M arrest in response to docetaxel treatment. These results show that inhibition of DRG2 expression can be useful to enhance docetaxel-induced apoptosis despite low-dose administration in castration-resistant prostate cancer.

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Section: Discussioncontrasting

confidence: 94%

Section: Introductionmentioning

confidence: 99%

Developmentally regulated GTP-binding protein 2 levels in prostate cancer cell lines impact docetaxel-induced apoptosis

et al. 2021

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“…In addition, there were several genes identified that were significantly under-expressed in IDH1-mutant astrocytoma compared to IDH1-wildtype. DRG2, developmentally regulated GTP-binding protein 2, has been shown to promote tumor growth and metastasis [ 120 , 121 , 122 ]. Depletion or inhibition of DRG2 was shown to promote survival in mice [ 122 ].…”

Section: Resultsmentioning

confidence: 99%

“…DRG2, developmentally regulated GTP-binding protein 2, has been shown to promote tumor growth and metastasis [ 120 , 121 , 122 ]. Depletion or inhibition of DRG2 was shown to promote survival in mice [ 122 ]. TRIP4, which is a thyroid hormone receptor interactor, also promotes cell proliferation and migration.…”

Section: Resultsmentioning

confidence: 99%

A Genome-Wide Profiling of Glioma Patients with an IDH1 Mutation Using the Catalogue of Somatic Mutations in Cancer Database

Pappula

Rasheed

Mirzaei

et al. 2021

Cancers

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Gliomas are differentiated into two major disease subtypes, astrocytoma or oligodendroglioma, which are then characterized as either IDH (isocitrate dehydrogenase)-wild type or IDH-mutant due to the dramatic differences in prognosis and overall survival. Here, we investigated the genetic background of IDH1-mutant gliomas using the Catalogue of Somatic Mutations in Cancer (COSMIC) database. In astrocytoma patients, we found that IDH1 is often co-mutated with TP53, ATRX, AMBRA1, PREX1, and NOTCH1, but not CHEK2, EGFR, PTEN, or the zinc finger transcription factor ZNF429. The majority of the mutations observed in these genes were further confirmed to be either drivers or pathogenic by the Cancer-Related Analysis of Variants Toolkit (CRAVAT). Gene expression analysis showed down-regulation of DRG2 and MSN expression, both of which promote cell proliferation and invasion. There was also significant over-expression of genes such as NDRG3 and KCNB1 in IDH1-mutant astrocytoma patients. We conclude that IDH1-mutant glioma is characterized by significant genetic changes that could contribute to a better prognosis in glioma patients.

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“…VEGF-A is an essential angiogenic growth factor that is a powerful promoter of the adhesion and proliferation of vascular endothelial cells (44,45). Hence, VEGF-A can regulate the development of various cancers including liver cancer, colorectal cancer, melanoma and lung cancer (46)(47)(48)(49). MiR-126 can inhibit the expression of sprouty-related EVH1 domain-containing gene 1 (SPRED), an inhibiting factor of the MAP kinase (MAPK) pathway, and the p3kr2 (PI3KR2/p85-b) gene, a subunit of PI3K (50-52).…”

Section: Mir-126 and Lung Cancer Tumorigenesismentioning

confidence: 99%

MicroRNA‑126: A new and promising player in lung cancer (Review)

Chen

Zhao

et al. 2020

Oncol Lett

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Lung cancer is one of the most common malignant tumors associated with cancer death; however, the mechanisms involved in lung tumor development have not been completely elucidated, which impedes the advancement of clinical diagnosis and therapy. MicroRNA-126 (miR-126) is an important member of the microRNA family and is encoded by intron 7 of epidermal growth factor-like domain-containing gene 7. Increasing evidence has demonstrated that miR-126, as a distinct endothelial-enriched miRNA and new tumor suppressor gene, serves a promising role in the occurrence, development and metastasis of various types of cancer, including liver cancer, colorectal cancer, melanoma and lung cancer. In the present review, the current knowledge of the role of miR-126 in lung cancer growth, metastasis, diagnosis and prognosis as well as therapy was summarized, which may provide new insights on the biological roles of miRNAsin lung cancer and facilitate the ultimate development of miRNA-based therapies in clinical patients with non-small cell lung cancer.

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DRG2 supports the growth of primary tumors and metastases of melanoma by enhancing VEGF‐A expression

Cited by 11 publications

References 48 publications

Developmentally regulated GTP-binding protein 2 levels in prostate cancer cell lines impact docetaxel-induced apoptosis

Developmentally regulated GTP-binding protein 2 levels in prostate cancer cell lines impact docetaxel-induced apoptosis

A Genome-Wide Profiling of Glioma Patients with an IDH1 Mutation Using the Catalogue of Somatic Mutations in Cancer Database

MicroRNA‑126: A new and promising player in lung cancer (Review)

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