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Conference Paper: DEPDC1B functions as an oncogene in promoting melanoma growth and metastasis

TitleDEPDC1B functions as an oncogene in promoting melanoma growth and metastasis
Authors
Issue Date2021
PublisherAmerican Association for Cancer Research. The Journal's web site is located at http://cancerres.aacrjournals.org/
Citation
Proceedings of the American Association for Cancer Research (AACR) Annual Meeting 2021, Virtual Meeting; 10-15 April 2021. In Cancer Research, 2021, v. 81 n. 13, Suppl., Abstract no. 2858 How to Cite?
AbstractBackground: Melanoma is one of the most aggressive skin cancers due to its therapeutic resistance, and high capacity to metastasize as a late manifestation. The limited effectiveness of the current treatment regimen prompts us to identify new druggable targets in governing the systemic spread of melanoma. Despite the oncogenic role of DEPDC1B in different types of cancer, its functional importance in melanoma growth and metastasis are not fully revealed. Methods: The expression of DEPDC1B mRNA levels between skin cutaneous melanoma patients and normal samples were compared using TCGA database. Surgically procured tumor specimens from melanoma patients were obtained to investigate the protein levels of DEPDC1B expression by immunofluorescence. Melanoma cell lines WM266-4 and SK-MEL-28 were used for loss- and gain-of-function studies of DEPDC1B in alamarblue, EdU staining, colony formation and trans-well invasion assays. Subcutaneous and intravenous injection of melanoma cells treated with either DEPDC1B knockdown (KD) or DEPDC1B overexpression into immunodeficient mice were conducted to examine the effects on tumor growth and lung metastasis respectively. Results: The expression levels of DEPDC1B mRNA in melanoma biopsies were higher than normal samples and were negatively corelated with both overall survival and disease-free survival. Loss-of-function studies showed that DEPDC1B KD reduced the growth rate, proliferation capacity and colony formation ability of melanoma cells. Consistently, DEPDC1B KD cells gave rise to smaller xenograft tumors and fewer number of lung nodules. In contrast, DEPDC1B overexpression promoted melanoma cell proliferation, colony formation and invasion in vitro, and enhanced xenograft tumor growth and lung metastasis. Conclusion: The results obtained so far indicate that DEPDC1B acts as an oncogene in promoting melanoma cell growth and metastasis, suggesting a potential drug target in melanoma treatment.
DescriptionPoster Session PO.TB04.01 - Invasion and Metastasis 1 - Abstract 2858
Persistent Identifierhttp://hdl.handle.net/10722/300583
ISSN
2023 Impact Factor: 12.5
2023 SCImago Journal Rankings: 3.468

 

DC FieldValueLanguage
dc.contributor.authorHu, F-
dc.contributor.authorFong, KO-
dc.contributor.authorCheung, MPL-
dc.contributor.authorYang, X-
dc.contributor.authorCheung, MCH-
dc.date.accessioned2021-06-18T14:54:05Z-
dc.date.available2021-06-18T14:54:05Z-
dc.date.issued2021-
dc.identifier.citationProceedings of the American Association for Cancer Research (AACR) Annual Meeting 2021, Virtual Meeting; 10-15 April 2021. In Cancer Research, 2021, v. 81 n. 13, Suppl., Abstract no. 2858-
dc.identifier.issn0008-5472-
dc.identifier.urihttp://hdl.handle.net/10722/300583-
dc.descriptionPoster Session PO.TB04.01 - Invasion and Metastasis 1 - Abstract 2858-
dc.description.abstractBackground: Melanoma is one of the most aggressive skin cancers due to its therapeutic resistance, and high capacity to metastasize as a late manifestation. The limited effectiveness of the current treatment regimen prompts us to identify new druggable targets in governing the systemic spread of melanoma. Despite the oncogenic role of DEPDC1B in different types of cancer, its functional importance in melanoma growth and metastasis are not fully revealed. Methods: The expression of DEPDC1B mRNA levels between skin cutaneous melanoma patients and normal samples were compared using TCGA database. Surgically procured tumor specimens from melanoma patients were obtained to investigate the protein levels of DEPDC1B expression by immunofluorescence. Melanoma cell lines WM266-4 and SK-MEL-28 were used for loss- and gain-of-function studies of DEPDC1B in alamarblue, EdU staining, colony formation and trans-well invasion assays. Subcutaneous and intravenous injection of melanoma cells treated with either DEPDC1B knockdown (KD) or DEPDC1B overexpression into immunodeficient mice were conducted to examine the effects on tumor growth and lung metastasis respectively. Results: The expression levels of DEPDC1B mRNA in melanoma biopsies were higher than normal samples and were negatively corelated with both overall survival and disease-free survival. Loss-of-function studies showed that DEPDC1B KD reduced the growth rate, proliferation capacity and colony formation ability of melanoma cells. Consistently, DEPDC1B KD cells gave rise to smaller xenograft tumors and fewer number of lung nodules. In contrast, DEPDC1B overexpression promoted melanoma cell proliferation, colony formation and invasion in vitro, and enhanced xenograft tumor growth and lung metastasis. Conclusion: The results obtained so far indicate that DEPDC1B acts as an oncogene in promoting melanoma cell growth and metastasis, suggesting a potential drug target in melanoma treatment.-
dc.languageeng-
dc.publisherAmerican Association for Cancer Research. The Journal's web site is located at http://cancerres.aacrjournals.org/-
dc.relation.ispartofCancer Research-
dc.relation.ispartofAmerican Association for Cancer Research (AACR) Virtual Meeting I-
dc.titleDEPDC1B functions as an oncogene in promoting melanoma growth and metastasis-
dc.typeConference_Paper-
dc.identifier.emailCheung, MPL: mplcheun@hku.hk-
dc.identifier.emailCheung, MCH: mcheung9@hku.hk-
dc.identifier.authorityCheung, MCH=rp00245-
dc.description.natureabstract-
dc.identifier.doi10.1158/1538-7445.AM2021-2858-
dc.identifier.hkuros323012-
dc.identifier.volume81-
dc.identifier.issue13, Suppl.-
dc.identifier.spageAbstract nr 2858-
dc.identifier.epageAbstract nr 2858-
dc.publisher.placeUnited States-

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