Epigenetic Mechanisms Underlying the Dynamic Expression of Cancer-Testis Genes, PAGE2, -2B and SPANX-B, during Mesenchymal-to-Epithelial Transition

Yilmaz-Ozcan, Sinem; Sade, Asli; Kucukkaraduman, Baris; Kaygusuz, Yasemin; Senses, Kerem Mert; Banerjee, Sreeparna; Gure, Ali Osmay

doi:10.1371/journal.pone.0107905

Cited by 15 publications

(8 citation statements)

References 41 publications

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“…This group of CTAg has documented immunogenicity ( 16 ) and their expression is found at higher levels in more aggressive tumors ( 17 ). A range of CTAg (including SPANX and a number of MAGE family members) were also recently shown to be upregulated following EMT in a colorectal cancer cell line ( 18 ).…”

Section: Introductionmentioning

confidence: 99%

Effects of Epithelial to Mesenchymal Transition on T Cell Targeting of Melanoma Cells

et al. 2014

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Melanoma cells can switch phenotype in a manner similar to epithelial to mesenchymal transition (EMT). In this perspective article, we address the effects of such phenotype switching on T cell targeting of tumor cells. During the EMT-like switch in phenotype, a concomitant change in expression of multiple tumor antigens occurs. Melanoma cells undergoing EMT escape from killing by T cells specific for antigens whose expression is downregulated by this process. We discuss melanoma antigens whose expression is influenced by EMT. We assess the effect of changes in the expressed tumor antigen repertoire on T-cell mediated tumor recognition and killing. In addition to escape from T cell immunity via changes in antigen expression, mesenchymal-like melanoma cells are generally more resistant to classical chemotherapy and radiotherapy. However, we demonstrate that when targeting antigens whose expression is unaltered during EMT, the capacity of T cells to kill melanoma cell lines in vitro is not influenced by their phenotype. When considering immune therapies such as cancer vaccination, these data suggest escape from T cell killing due to phenotype switching in melanoma could potentially be avoided by careful selection of target antigen.

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Section: Introductionmentioning

confidence: 99%

Effects of Epithelial to Mesenchymal Transition on T Cell Targeting of Melanoma Cells

et al. 2014

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“…To our knowledge, in vitro studies of the role of SPANXN2 in TGCT have not yet been reported and it is not clear if SPANXN2 acts as a tumor suppressor gene or oncogene in TGCT. Previous studies have shown abnormal SPANX gene expression in many cancers, which may promote or inhibit tumor invasion (Yilmaz-Ozcan et al, 2014;Maine et al, 2016). However, the role of SPANXN2 in TGCTs progression has not yet been elucidated.…”

Section: Discussionmentioning

confidence: 99%

SPANXN2 functions a cell migration inhibitor in testicular germ cell tumor cells

Zhu

Liu

et al. 2020

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Background SPANX family members are thought to play an important role in cancer progression. The SPANXN2 is a gene expressed mainly in normal testis, but its role in testicular germ cell tumors (TGCTs) has yet to be investigated. TGCT is one of the most common solid tumors in young men and is associated with poor prognosis; however, effective prognostic indicators remain elusive. Therefore, we investigated the role of SPANXN2 in TGCT development. Methods SPANXN2 expression levels were validated by quantitative real-time polymerase chain reaction (qRT-PCR) analyses of 14 TGCT samples and five adjacent normal tissue samples. SPANXN2 was transiently overexpressed in TGCT cells to study the consequences for cell function. The effects of SPANXN2 on cell migration were evaluated in transwell and wound healing assays. The effects on cloning ability were evaluated in colony formation assays. MTT assays and cell cycle analysis were used to detect the effects of SPANXN2 on cell proliferation. The expression levels of EMT- and AKT-related proteins in cells overexpressing SPANXN2 were analyzed by Western blotting. Results Compared with adjacent normal tissues, the Gene Expression Profiling Interactive Analysis database showed SPANXN2 expression was downregulated in TGCTs which was consistent with the qRT-PCR analysis. SPANXN2 overexpression reduced cell migration and colony formation capability and downregulated expression of EMT- and AKT-related proteins, Vimentin, Snail, AKT, and p-AKT. Conclusion Our results suggest that SPANXN2 regulates TGCT cell migration via EMT- and AKT-related proteins although its role in the occurrence and development of TGCT remains to be fully elucidated.

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Section: Discussionmentioning

confidence: 99%

Peer Review #1 of "SPANXN2 functions a cell migration inhibitor in testicular germ cell tumor cells (v0.1)"

2020

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Background: SPANX family members are thought to play an important role in cancer progression. The SPANXN2 is a gene expressed mainly in normal testis, but its role in testicular germ cell tumors (TGCTs) has yet to be investigated. TGCT is one of the most common solid tumors in young men and is associated with poor prognosis; however, effective prognostic indicators remain elusive. Therefore, we investigated the role of SPANXN2 in TGCT development. Methods: SPANXN2 expression levels were validated by quantitative real-time polymerase chain reaction (qRT-PCR) analyses of 14 TGCTs samples and five adjacent normal tissue samples. SPANXN2 was transiently overexpressed in TGCT cells to study the consequences for cell function. The effects of SPANXN2 on cell migration were evaluated in transwell and wound healing assays. The effects on cloning ability were evaluated in colony formation assays. MTT assays and cell cycle analysis were used to detect the effects of SPANXN2 on cell proliferation. The expression levels of EMT-and AKTrelated proteins in cells overexpressing SPANXN2 were analyzed by Western blotting. Results: Compared with adjacent normal tissues, the Gene Expression Profiling Interactive Analysis database showed SPANXN2 expression was downregulated in TGCTs which was consistent with the qRT-PCR analysis. SPANXN2 overexpression reduced cell migration and colony formation capability and downregulated expression of EMT-and AKT-related proteins, Vimentin, Snail, AKT, and p-AKT. Conclusion: Our results suggest that SPANXN2 regulates TGCT cell migration via EMT-and AKT-related proteins although its role in the occurrence and development of TGCT remains to be fully elucidated.

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Epigenetic Mechanisms Underlying the Dynamic Expression of Cancer-Testis Genes, PAGE2, -2B and SPANX-B, during Mesenchymal-to-Epithelial Transition

Cited by 15 publications

References 41 publications

Effects of Epithelial to Mesenchymal Transition on T Cell Targeting of Melanoma Cells

Effects of Epithelial to Mesenchymal Transition on T Cell Targeting of Melanoma Cells

SPANXN2 functions a cell migration inhibitor in testicular germ cell tumor cells

Peer Review #1 of "SPANXN2 functions a cell migration inhibitor in testicular germ cell tumor cells (v0.1)"

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