The novel protein C9orf116 promotes rat liver cell line BRL-3A proliferation

Zhang, Chunyan; Chang, Cuifang; Zhao, Weihua; Gao, Hang; Wang, Qiwen; Liu, Deming; Zhang, Fuchun; Zhang, Shifu; Xu, Chi

doi:10.1371/journal.pone.0180607

Cited by 3 publications

(6 citation statements)

References 43 publications

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“…According to the bioinformatics data, the expression level of PIERCE1 was increased in patients with CRC, similar to the previous report of its proliferation-enhancing role in cell lines derived from different tissue types [ 26 ]. While our studies were conducted to examine the oncogenic role of PIERCE1, it did not increase cancer cell proliferation or tumor progression in CRC models.…”

Section: Discussionsupporting

confidence: 86%

“…By far the signal transduction linked to PIERCE1 is E2F1, TP53, ATR, CCNA2, CCND1, c-MYC, NODAL, LEFTY1/2, PITX2, CERL2, RENIN, ATP6AP2 [ 21 , 22 , 24 , 25 , 26 ], which are closely related to ciliogenesis, cell cycle, DNA repair, and cancer. However, according to our data, it is likely that PIERCE1 and APC/KRAS cannot synergize to affect more aggressive tumorigenesis in mice and human cell lines.…”

Section: Discussionmentioning

confidence: 99%

“…Furthermore, it is frequently down-regulated in immortalized cells and expressed in a cell cycle-dependent manner, playing an important role in the S or G2 phase [ 25 ]. A recent study showed that PIERCE1 induced proliferation of rat liver cell line BRL-3A by modulating cell cycle transition and the expressions of CCNA2, CCND1, and MYC [ 26 ], thereby suggesting an oncogenic role.…”

Section: Introductionmentioning

confidence: 99%

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Effect of PIERCE1 on colorectal cancer

Park

Kim

et al. 2020

Exp. Anim.

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Colorectal cancer is the second most lethal cancer type across all ages and sexes, the many mechanisms of which are still currently being further elucidated. PIERCE1 has been known to be involved in the cell cycle and proliferation, the expression of which is regulated by stress conditions in a p53-dependent manner. Through a database search, we found that PIERCE1 was significantly augmented in patients with colorectal carcinoma compared to normal samples, suggesting its possible role in tumor regulation. Recently, PIERCE1 has also been reported to increase proliferation of a liver cancer cell line, indicating its possible role as an oncogene. To examine its relevance to tumorigenesis, such as whether it has either oncogenic or tumor suppressive function, PIERCE1 was knocked down and overexpressed in several colorectal cancer cell lines and mice, respectively. To evaluate the roles of Pierce1 in vivo , we established a Pierce1 transgenic (TG) mouse model and then administered azoxymethane with dextran sodium sulfate (DSS) to induce colorectal carcinogenesis via promoting mutations in Apc and Kras . Nonetheless, PIERCE1 depletion in these cell lines showed no significant change in cell growth. AOM/DSS-treated Pierce1 TG mice were comparable with respect to colon lengths, the number of polyps, and tumor sizes to those of the control mice. These results implicate that PIERCE1 does not play an oncogenic or tumor suppressive role in AOM/DSS-induced colorectal cancer.

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Section: Discussionsupporting

confidence: 86%

Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Effect of PIERCE1 on colorectal cancer

Park

Kim

et al. 2020

Exp. Anim.

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“…PIERCE1 is a tumor-associated protein that promotes cell proliferation and controls cell death under stress conditions [2,4]. The cancer promoting activity and lung-specific expression of PIERCE1 prompted us to examine the link between PIERCE1 and lung cancer.…”

Section: Pierce1 Promotes Cell Growth Especially In Krasmutant Lung Cmentioning

confidence: 99%

“…Genotoxic stresses, such as ultraviolet C (UVC), can induce PIERCE1 expression and stabilize its protein by proteasome inhibitor treatment [ 2 ]. A recent report showed enhanced cell proliferation with upregulation of cyclin A2 (CCNA2), cyclin D1 (CCND1), and MYC expressions by overexpression of PIERCE1 in rat liver cells [ 4 ]. This suggests that PIERCE1 modulates cell cycle transition and proliferation during tumorigenesis.…”

Section: Introductionmentioning

confidence: 99%

Impaired AKT signaling and lung tumorigenesis by PIERCE1 ablation in KRAS-mutant non-small cell lung cancer

et al. 2020

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KRAS-mutant non-small cell lung cancer (NSCLC) is a major lung cancer subtype that leads to many cancer-related deaths worldwide. Although numerous studies on KRAS-mutant type NSCLC have been conducted, new oncogenic or tumor suppressive genes need to be detected because a large proportion of NSCLC patients does not respond to currently used therapeutics. Here, we show the tumor-promoting function of a cell cycle-related protein, PIERCE1, in KRAS-mutant NSCLC. Mechanistically, PIERCE1 depletion inhibits cell growth and AKT phosphorylation (pAKT) at S473, which is particularly observed in KRAS-mutant lung cancers. Analyses of AKT-related genes using microarray, immunoblotting, and real-time quantitative PCR indicated that PIERCE1 negatively regulates the gene expression of the AKT suppressor, TRIB3, through the CHOP pathway, which is a key regulatory pathway for TRIB3 expression. Similarly, in vivo analyses of PIERCE1 depletion in the KRAS mutation-related lung cancer mouse models revealed the suppressive effect of PIERCE1 knockout in urethane-and KRAS G12D-induced lung tumorigenesis with decreased pAKT levels observed in the tumors. Tissue microarrays of human lung cancers indicated the expression of PIERCE1 in 83% of lung cancers and its correlation with pAKT expression. Thus, we illustrate how PIERCE1 depletion may serve as a therapeutic strategy against KRASmutant NSCLC and propose the clinical benefit of PIERCE1.

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Identification of Subtype-Specific Prognostic Biomarkers in Breast Cancer

Esfahani¹,

Ghezlou

Moghaddam

et al. 2022

Preprint

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Breast cancer (BC) is a heterogeneous disease divided into four molecular subtypes that display different prognoses. Molecular alterations in breast cells contribute to breast carcinogenesis. However, the molecular characteristics involved in developing BC subtypes remain largely unknown. Further identification of molecular mechanisms involved in different BC subtypes might help improve treatment strategies and prognosis of patients. In the present study, two microarray datasets (GSE57297 and GSE65194) containing four BC subtypes were downloaded from the Gene Expression Omnibus (GEO) database. Comparative analyses were performed to identify specific differentially expressed genes (DEGs) for each BC subtype, as well as overlapped (core) between all subtypes. bc-GenExMiner and Kaplan-Meier plotter databases were respectively utilized to investigate the differential expression and prognostic value of DEGs. A total of 25 DEGs (12 specific and 13 core) were found to be significantly associated with prognosis. We found that a high level of C9orf116 predicted better OS in the Luminal A subtype. Also, increased transcription levels of FAM13A and RASIP1 were associated with shorter OS in the Luminal B subtype. High mRNA expression of PDE7A, and COTL1 conferred longer OS, while elevated expression of TM4SF1 and AREG predicted shorter OS in the TNBC subtype. Increased mRNA levels of GSR, and DAPK2 conferred better OS in the HER2 subtype; however, increased expression levels of HOTAIR, PLEKHG4, and POU6F1 predicted poor OS. For the core DEGs, increased expression of IFI6 and UBE2S predicted shorter OS. Meanwhile, increased mRNA levels of AK5, C2orf40, CNN1, HOXA5, NTRK2, PAMR1, PROS1, SCARA5, SDPR, TGFBR3, and TSHZ2 conferred better OS. In conclusion, this study strictly identified specific genes that may help to select precision prognostic biomarkers in different BC subtypes.

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The novel protein C9orf116 promotes rat liver cell line BRL-3A proliferation

Cited by 3 publications

References 43 publications

Effect of PIERCE1 on colorectal cancer

Effect of PIERCE1 on colorectal cancer

Impaired AKT signaling and lung tumorigenesis by PIERCE1 ablation in KRAS-mutant non-small cell lung cancer

Identification of Subtype-Specific Prognostic Biomarkers in Breast Cancer

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