PDCD2 functions in cancer cell proliferation and predicts relapsed leukemia

Barboza, Nora M.; Minakhina, Svetlana; Medina, Daniel; Balsara, Binaifer; Greenwood, Sonya; Huzzy, Lien; Rabson, Arnold B.; Steward, Ruth; Schaar, Dale

doi:10.4161/cbt.24484

Cited by 20 publications

(35 citation statements)

References 26 publications

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“…In addition to PDCD5, other programmed cell death proteins are also known to play important roles in apoptosis and/or cell cycle progression (54)(55)(56)(57), and are also dysregulated in many types of human cancers (13,16,(58)(59)(60)(61)(62)(63). Opposite to what we observed for PDCD5, depletion of PDCD2 in human acute leukemia cells impairs their proliferation, induces cell cycle arrest and p53 activation while overexpression of PDCD2 facilitates cell growth in cancers (55,64). However, in gastric cancer cells, expression of PDCD2 seems to induce cell cycle arrest and apoptosis, which are also found to be p53-dependent (54).…”

Section: Discussionmentioning

confidence: 51%

PDCD5 regulates cell proliferation, cell cycle progression and apoptosi

Hong-xin

Wang

et al. 2017

Oncol Lett

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Abstract. Programmed cell death (PDCD)5 is cloned from human leukemia cell line TF-1. PDCD5 is one of the members of the programmed cell death protein family that is frequently involved in tumor growth and apoptosis. To investigate the molecular and cellular functions of PDCD5, the present study established a PDCD5 stably overexpressing A431 cell line and examined the role of PDCD5 in cell proliferation, cell cycle progression and apoptosis. The data demonstrated that overexpression of PDCD5 significantly inhibited cell proliferation, induced cell cycle arrest at G2/M phase and apoptosis in A431 cells. The expression profiles of certain key regulators of these cellular events were further investigated, including P53, B cell lymphoma (BCL)-2, BCL-2 associated X protein (BAX) and caspase (CASP)3. The data demonstrated that at the transcript and protein levels, P53, BAX and CASP3 were all upregulated in the PDCD5 stably overexpressing A431 cells whereas BCL-2 was downregulated, indicating that PDCD5 acts as an important upstream regulator of P53, BCL-2, BAX and CASP3. The data suggest that PDCD5 regulates cell proliferation, cell cycle progression and apoptosis in A431 cells. PDCD5 may be a novel tumor suppressor gene, and may be potentially used for cancer treatment in the future.

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Section: Discussionmentioning

confidence: 51%

PDCD5 regulates cell proliferation, cell cycle progression and apoptosi

Hong-xin

Wang

et al. 2017

Oncol Lett

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“…Baron et al (12) showed that PDCD2 expression induces apoptosis of human erythroleukemia cells via activation of caspases. Barboza et al (13) reported that knockdown of PDCD2 expression in two different cancer cell lines (leukemia Jurkat cells and lung cancer A549 cells) significantly impairs cell proliferation and cell progression to S phase of the cell cycle. In the present study, we confirmed that PDCD2 expression induced apoptosis and S phase arrest in p53-expressing gastric cancer cells.…”

Section: Discussionmentioning

confidence: 99%

Programmed cell death 2 protein induces gastric cancer cell growth arrest at the early S phase of the cell cycle and apoptosis in a p53-dependent manner

et al. 2014

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Abstract. Programmed cell death 2 (PDCD2) is a highly conserved nuclear protein, and aberrant PDCD2 expression alters cell apoptosis. The present study aimed to investigate PDCD2 expression in gastric cancer. Tissue specimens from 34 gastric cancer patients were collected for analysis of PDCD2 expression using immunohistochemistry, western blotting and qRT-PCR. Gastric cancer cell lines (a p53-mutated MKN28 line and a wild-type p53 MKN45 line) were used to assess the effects of PDCD2 overexpression. p53 -/-nude mice were used to investigate the effect of PDCD2 on ultraviolet B (UVB)-induced skin carcinogenesis. The data showed that PDCD2 expression was reduced in gastric cancer tissue specimens, and loss of PDCD2 expression was associated with the poor survival of patients. PDCD2 expression induced gastric cancer cell growth arrest at the early S phase of the cell cycle and apoptosis. The antitumor effects of PDCD2 expression were dependent on p53 expression in gastric cancer cells. Moreover, PDCD2 expression inhibited activity of the ATM/Chk1/2/p53 signaling pathway. In addition, PDCD2 expression suppressed UVB-induced skin carcinogenesis in p53 +/+ nude mice, but not in p53 -/-mice. The data from the present study demonstrated that loss of PDCD2 expression could contribute to gastric cancer development and progression and that PDCD2-induced gastric cancer cell growth arrest at the early S phase of the cell cycle and apoptosis are p53-dependent.

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“…To do so, we examined the capability of Zfrp8 deletion constructs to rescue mutant lethality. Expression of human PDCD2 cDNAs driven by the general driver da-Gal4 is fully capable of rescuing Zfrp8 lethality (Barboza et al, 2013; Minakhina et al, 2014). We created mutated Zfrp8 constructs, removing either the two putative NLSs or the putative NES domains.…”

Section: Resultsmentioning

confidence: 99%

“…Similarly in vertebrates, the Zfrp8 homolog, Pdcd2 , is essential for embryonic stem cell maintenance and the growth of mouse embryonic fibroblasts; Pdcd2 mouse embryos die before implantation (Granier et al, 2014; Mu et al, 2010). PDCD2 is abundantly expressed and essential in highly proliferative cells including cultured cells and clinical isolates obtained from patients with hematologic malignancies (Barboza et al, 2013). The function of Zfrp8 and PDCD2 is highly conserved, as expression of transgenic PDCD2 is sufficient to rescue Zfrp8 phenotypes (Minakhina et al, 2014).…”

Section: Introductionmentioning

confidence: 99%

Zfrp8 forms a complex with fragile-X mental retardation protein and regulates its localization and function

Tan

Schauder

Naryshkina

et al. 2016

Developmental Biology

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Fragile-X syndrome is the most commonly inherited cause of autism and mental disabilities. The Fmr1 (Fragile-X Mental Retardation 1) gene is essential in humans and Drosophila for the maintenance of neural stem cells, and Fmr1 loss results in neurological and reproductive developmental defects in humans and flies. FMRP (Fragile-X Mental Retardation Protein) is a nucleo-cytoplasmic shuttling protein, involved in mRNA silencing and translational repression. Both Zfrp8 and Fmr1 have essential functions in the Drosophila ovary. In this study, we identified FMRP, Nufip (Nuclear Fragile-X Mental Retardation Protein-interacting Protein) and Tral (Trailer Hitch) as components of a Zfrp8 protein complex. We show that Zfrp8 is required in the nucleus, and controls localization of FMRP in the cytoplasm. In addition, we demonstrate that Zfrp8 genetically interacts with Fmr1 and tral in an antagonistic manner. Zfrp8 and FMRP both control heterochromatin packaging, also in opposite ways. We propose that Zfrp8 functions as a chaperone, controlling protein complexes involved in RNA processing in the nucleus.

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PDCD2 functions in cancer cell proliferation and predicts relapsed leukemia

Cited by 20 publications

References 26 publications

PDCD5 regulates cell proliferation, cell cycle progression and apoptosi

PDCD5 regulates cell proliferation, cell cycle progression and apoptosi

Programmed cell death 2 protein induces gastric cancer cell growth arrest at the early S phase of the cell cycle and apoptosis in a p53-dependent manner

Zfrp8 forms a complex with fragile-X mental retardation protein and regulates its localization and function

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