HnRNP E2 is downregulated in human oral cancer cells and the overexpression of <i>hnRNP E2</i> induces apoptosis

Roychoudhury, Paromita; Paul, Ranjan Rashmi; Chowdhury, Rajdeep; Chaudhuri, Keya

doi:10.1002/mc.20265

Cited by 24 publications

(14 citation statements)

References 32 publications

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“…Third, PCBP2 siRNA transfection into the glioma cells induced caspase-3-mediated apoptosis. The relationship between PCBP2 and apoptosis has also been investigated in oral cancer (14). Together, these results may explain how PCBP2 could affect glioblastoma progression in vivo.…”

Section: Discussionmentioning

confidence: 98%

“…It has been suggested that PCBP2 also plays an important role in human malignancies. However, in addition to its overexpression during leukomegenesis (13) and its underexpression in oral cancer (14), PCBP2 is one of the least studied proteins in human cancers among PCBPs. Most of the reports on PCBP2 have focused on its posttranscriptional and translational controls in RNA viruses.…”

Section: Introductionmentioning

confidence: 99%

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RNA-binding protein PCBP2 modulates glioma growth by regulating FHL3

Han¹,

Xin²,

Zhao³

et al. 2013

J. Clin. Invest.

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Section: Discussionmentioning

confidence: 98%

Section: Introductionmentioning

confidence: 99%

RNA-binding protein PCBP2 modulates glioma growth by regulating FHL3

Han¹,

Xin²,

Zhao³

et al. 2013

J. Clin. Invest.

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“…Notably, studies suggest that PCBP2 is involved in tumor development. For instance, PCBP2 expression is found to be high in leukemia and glioma (12,22) but low in oral cancer (23). However, the role of PCBP2 in tumorigenesis is not clear.…”

mentioning

confidence: 99%

RNA-binding Protein PCBP2 Regulates p73 Expression and p73-dependent Antioxidant Defense

Ren¹,

Zhang²,

Yan

et al. 2016

Journal of Biological Chemistry

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TAp73, a member of the p53 family tumor suppressors, plays a critical rule in tumor suppression and neuronal development. However, how p73 activity is controlled at the posttranscriptional level is not well understood. Here, we showed that TAp73 activity is regulated by RNA-binding protein PCBP2. Specifically, we found that knockdown or knock-out of PCBP2 reduces, whereas ectopic expression of PCBP2 increases, TAp73 expression. We also showed that PCBP2 is necessary for p73 mRNA stability via the CU-rich elements in p73 3 -UTR. To uncover the biological relevance of PCBP2-regulated TAp73 expression, we showed that ectopic expression of PCBP2 inhibits, whereas knockdown or knock-out of PCBP2 increases, the production of reactive oxygen species (ROS) in a TAp73-dependent manner. Additionally, we found that glutaminase 2 (GLS2), a modulator of p73-dependent antioxidant defense, is also involved in PCBP2-regulated ROS production. Moreover, we generated PCBP2-deficient mice and primary mouse embryonic fibroblasts (MEFs) and showed that loss of PCBP2 leads to decreased p73 expression and, subsequently, increased ROS production and accelerated cellular senescence. Together, our data suggest that PCBP2 regulates p73 expression via mRNA stability and p73-dependent biological function in ROS production and cellular senescence.p73, along with p53 and p63, consists of the p53 family and is expressed as multiple isoforms (1). Through alternative splicing, at least seven isoforms (␣, ␤, ␥, ␦, ⑀, , and ) are expressed. In addition, due to the usage of two different promoters, p73 is expressed as two different isoforms, TAp73 and ⌬Np73. The TAp73 isoform is transcribed from the upstream P1 promoter and contains an N-terminal activation domain conserved in p53, whereas the ⌬Np73 isoform is produced by the downstream P2 promoter and, thus, N-terminally truncated. Consequently, TAp73, like p53, regulates an array of genes for tumor suppression (2). Indeed, mice deficient in TAp73 are prone to spontaneous tumors and premature aging (3, 4). By contrast, ⌬Np73 acts as an oncoprotein against TAp73 as well as p53 (5, 6). For example, ⌬Np73 promotes cell immortalization in mouse embryonic fibroblasts (MEFs) 5 and cooperates with oncogenic Ras in cell transformation in vitro and in vivo (7). In addition, mice deficient in ⌬Np73 do not develop tumors but exhibit delayed onset of moderate neurodegeneration (8, 9). The opposing functions of TAp73 and ⌬Np73 create more complicated issues for the role of p73 in cancer. Therefore, it is important to understand how p73 expression is controlled, which would advance our understanding of p73 biology and shed light on the development of novel strategy for cancer management.The poly(rC)-binding protein 2 (PCBP2) is a RNA-binding protein and belongs to the PCBP family. Members of PCBP family are characterized by their affinity to single-stranded poly(C) motifs in their target mRNAs (10). PCBP2 is a multifunctional protein and regulates gene expression at multiple levels including mRNA metabolism an...

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“…18 Also, hnRNP E2 was found to be significantly downregulated in human oral cancer tissues. 19 Previously, we reported for the first time that hnRNP G has tumor suppressive effects in oral cancers. Here, archived oral mucosal tissues representing the full spectrum of in situ oral carcinogenesis were stained for hnRNP G protein expression by in situ immunohistochemistry.…”

Section: Discussionmentioning

confidence: 99%

Expression and mutation analysis of heterogeneous nuclear ribonucleoprotein G in human oral cancer

Shin¹,

Kim²,

Yu³

et al. 2011

Oral Oncology

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We previously reported that wild type (wt) hnRNP G exhibited tumor suppressive activity in human oral squamous cell carcinoma (HOSCC) cell lines lacking hnRNP G. Wt hnRNP G markedly inhibited the proliferation capacity, anchorage independency and in vivo tumorigencity of HOSCC cells and notably enhanced the DNA repair capabilities of these cells. In the present study, we studied the genetic and expression states of hnRNP G in normal, premalignant and malignant human oral tissues to further understand the relationship between the hnRNP G alterations and the development of human oral cancer. To correlate the cancer development and the level of hnRNP G expression, we performed an immunohistochemistry staining of hnRNP G in normal, premalignant and malignant human oral tissues. Moreover, we examined the entire coding regions of hnRNP G from selected samples to understand the cause of the alterations of the gene expression. The expression of hnRNP G was notably decreased or completely abolished in 80% of premalignant-dysplastic and malignant oral epithelial tissues, whereas 100% of normal and 90% of hyperplastic non-dysplastic epithelium showed high level of hnRNP G in the nucleus of the basal cell layers. Approximately 80% of HOSCC lacking the expression of hnRNP G showed genetic alteration in hnRNP G, i.e., point mutation and exonic deletion. This study suggest that genetic alterations and aberrant expression of hnRNP G occurring during oral carcinogenesis might be useful markers for the early detection of human oral cancer.

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HnRNP E2 is downregulated in human oral cancer cells and the overexpression of hnRNP E2 induces apoptosis

Cited by 24 publications

References 32 publications

RNA-binding protein PCBP2 modulates glioma growth by regulating FHL3

RNA-binding protein PCBP2 modulates glioma growth by regulating FHL3

RNA-binding Protein PCBP2 Regulates p73 Expression and p73-dependent Antioxidant Defense

Expression and mutation analysis of heterogeneous nuclear ribonucleoprotein G in human oral cancer

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