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Conference Paper: The tumor suppressive role of PRMT6 in regulating the pathogenesis of hepatocellular carcinoma

TitleThe tumor suppressive role of PRMT6 in regulating the pathogenesis of hepatocellular carcinoma
Authors
KeywordsMedical sciences
Oncology
Issue Date2015
PublisherAmerican Association for Cancer Research. The Journal's web site is located at http://cancerres.aacrjournals.org/
Citation
The 106th Annual Meeting of the American Association for Cancer Research (AACR 2015), Philadelphia, PA., 18-22 April 2015. In Cancer Research, 2015, v. 75, n. 15 suppl., abstract no. 2333 How to Cite?
AbstractHepatocellular carcinoma (HCC) is the most common primary malignancy of the liver. The overall 5-year survival rate of HCC patients remains at a dismal 15% due to late diagnosis, metastasis and frequent tumor relapse. The presence of cancer stem cells (CSCs) has been proposed to account partly for the challenge of treating HCC. Our group has previously identified CD133 as a functional CSC marker of HCC. By adopting a PCR array encompassing diverse human chromatin modifiers, protein arginine methyltransferase 6 (PRMT6) was found to be differentially down-regulated in CD133+ human HCC cells. 55.8% (43/77) of clinical HCC tumor tissues showed down-regulated PRMT6 expression and patients with reduced PRMT6 expression were at significant risk of disrupted tumor encapsulation and manifested vascular invasion. An antagonistic relationship between PRMT6 and CD133 was observed in HCC cells, while modulation of PRMT6 led to an inversely altered CD133 expression. PRMT6 knockdown in liver cancer cells induced morphological alterations, where extensive cytoplasmic stretching and filopodia-like projections were observed. Moreover, PRMT6 regulated cancer and stem cell-like properties in vitro and in vivo including proliferation, colony formation, invasion, migration, angiogenesis, self-renewal, chemo-sensitivity and tumor initiation. In addition, stable knockdown of CD133 in HCC cells did not alter PRMT6 expression levels, which suggested that PRMT6 is potentially functioning upstream of CD133. Ongoing studies are in progress to delineate the underlying mechanisms by which PRMT6 suppress HCC.
DescriptionThis journal suppl. entitled: Proceedings: AACR 106th Annual Meeting 2015; April 18-22, 2015; Philadelphia, PA
Persistent Identifierhttp://hdl.handle.net/10722/214995
ISSN
2015 Impact Factor: 8.556
2015 SCImago Journal Rankings: 5.372

 

DC FieldValueLanguage
dc.contributor.authorChan, LH-
dc.contributor.authorNg, KY-
dc.contributor.authorMa, S-
dc.date.accessioned2015-08-21T12:17:27Z-
dc.date.available2015-08-21T12:17:27Z-
dc.date.issued2015-
dc.identifier.citationThe 106th Annual Meeting of the American Association for Cancer Research (AACR 2015), Philadelphia, PA., 18-22 April 2015. In Cancer Research, 2015, v. 75, n. 15 suppl., abstract no. 2333-
dc.identifier.issn0008-5472-
dc.identifier.urihttp://hdl.handle.net/10722/214995-
dc.descriptionThis journal suppl. entitled: Proceedings: AACR 106th Annual Meeting 2015; April 18-22, 2015; Philadelphia, PA-
dc.description.abstractHepatocellular carcinoma (HCC) is the most common primary malignancy of the liver. The overall 5-year survival rate of HCC patients remains at a dismal 15% due to late diagnosis, metastasis and frequent tumor relapse. The presence of cancer stem cells (CSCs) has been proposed to account partly for the challenge of treating HCC. Our group has previously identified CD133 as a functional CSC marker of HCC. By adopting a PCR array encompassing diverse human chromatin modifiers, protein arginine methyltransferase 6 (PRMT6) was found to be differentially down-regulated in CD133+ human HCC cells. 55.8% (43/77) of clinical HCC tumor tissues showed down-regulated PRMT6 expression and patients with reduced PRMT6 expression were at significant risk of disrupted tumor encapsulation and manifested vascular invasion. An antagonistic relationship between PRMT6 and CD133 was observed in HCC cells, while modulation of PRMT6 led to an inversely altered CD133 expression. PRMT6 knockdown in liver cancer cells induced morphological alterations, where extensive cytoplasmic stretching and filopodia-like projections were observed. Moreover, PRMT6 regulated cancer and stem cell-like properties in vitro and in vivo including proliferation, colony formation, invasion, migration, angiogenesis, self-renewal, chemo-sensitivity and tumor initiation. In addition, stable knockdown of CD133 in HCC cells did not alter PRMT6 expression levels, which suggested that PRMT6 is potentially functioning upstream of CD133. Ongoing studies are in progress to delineate the underlying mechanisms by which PRMT6 suppress HCC.-
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.subjectMedical sciences-
dc.subjectOncology-
dc.titleThe tumor suppressive role of PRMT6 in regulating the pathogenesis of hepatocellular carcinoma-
dc.typeConference_Paper-
dc.identifier.emailNg, KY: jkyng@hku.hk-
dc.identifier.emailMa, S: stefma@hku.hk-
dc.identifier.authorityMa, S=rp00506-
dc.identifier.hkuros248962-
dc.identifier.volume75-
dc.identifier.issue15 suppl.-
dc.publisher.placeUnited States-

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