RANBP9 suppresses tumor proliferation in colorectal cancer

Qin, Chunzhi; Zhang, Qin; Wu, Guangbin

doi:10.3892/ol.2019.10134

Cited by 6 publications

(10 citation statements)

References 31 publications

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“…Reduced expression of RANBP9 has been associated with distant metastasis and chemo-resistance in gastric cancer [44] . The silencing of RANBP9 in colorectal cancer cells also resulted in an increase of cell growth in vitro and tumorigenesis in vivo [45] . However, a straightforward cancer suppressive role is clearly inconsistent with the ability of RANBP9 to enhance Receptor Tyrosine Kinases or MAPK signaling [46][47][48][49] .…”

Section: Ranbp9 and Cancermentioning

confidence: 96%

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RANBP9 as potential therapeutic target in non-small cell lung cancer

Tessari

Soliman

Orlacchio

et al. 2020

JCMT

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Non-small cell lung cancer (NSCLC) remains the leading cause of cancer-related deaths in the Western world. Despite progress made with targeted therapies and immune checkpoint inhibitors, the vast majority of patients have to undergo chemotherapy with platinum-based drugs. To increase efficacy and reduce potential side effects, a more comprehensive understanding of the mechanisms of the DNA damage response (DDR) is required. We have shown that overexpressby live cell imaging (Incuyion of the scaffold protein RAN binding protein 9 (RANBP9) is pervasive in NSCLC. More importantly, patients with higher levels of RANBP9 exhibit a worse outcome from treatment with platinum-based drugs. Mechanistically, RANBP9 exists as a target and an enabler of the ataxia telangiectasia mutated (ATM) kinase signaling. Indeed, the depletion of RANBP9 in NSCLC cells abates ATM activation and its downstream targets such as pby live cell imaging (Incuy53 signaling. RANBP9 knockout cells are more sensitive than controls to the inhibition of the ataxia and telangiectasia-related (ATR) kinase but not to ATM inhibition. The absence of RANBP9 renders cells more sensitive to drugs inhibiting the Poly(ADP-ribose)-Polymerase (PARP) resulting in a "BRCAness-like" phenotype. In summary, as a result of increased sensitivity to DNA damaging drugs conferred by its ablation in vitro and in vivo , RANBP9 may be considered as a potential target for the treatment of NSCLC. This article aims to report the results from past and ongoing investigations focused on the role of RANBP9 in the response to DNA damage, particularly in the context of NSCLC. This review concludes with future directions and speculative remarks which will need to be addressed in the coming years.

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Section: Ranbp9 and Cancermentioning

confidence: 96%

“…While it remains unclear whether RANBP9's tumor suppressive effects is observed in vitro, most studies agree that RANBP9 is over-expressed in a variety of highly prevalent tumor types including that of NSCLC [44,45,[50][51][52] .…”

Section: Ranbp9 and Cancermentioning

confidence: 99%

RANBP9 as potential therapeutic target in non-small cell lung cancer

Tessari

Soliman

Orlacchio

et al. 2020

JCMT

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“…The study by Qin et al recently reported that both RANBP9 mRNA and protein expression are increased in colorectal cancer compared to paired normal mucosa. However, in vitro and in xenografts from HCT116 and HT29 knockdown of RANBP9 resulted in increased proliferation [66].…”

Section: Ctlh Complex Members: Tumor Suppressors or Oncogenes? Drimentioning

confidence: 99%

“…Despite the in vitro evidence showing that knockdown of RANBP9 results in increased tumor cell proliferation, invariably, tumors of different types display higher levels of expression compared to the normal counterpart. This is true for lung cancer [65, 81], colorectal cancer [66], osteosarcoma [82], gastric cancer [64], and invasive breast cancer [83].…”

Section: Ctlh Complex Members: Tumor Suppressors or Oncogenes? Drimentioning

confidence: 99%

The CTLH Complex in Cancer Cell Plasticity

Huffman

Palmieri

Coppola

2019

Journal of Oncology

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Cancer cell plasticity is the ability of cancer cells to intermittently morph into different fittest phenotypic states. Due to the intrinsic capacity to change their composition and interactions, protein macromolecular complexes are the ideal instruments for transient transformation. This review focuses on a poorly studied mammalian macromolecular complex called the CTLH (carboxy-terminal to LisH) complex. Currently, this macrostructure includes 11 known members (ARMC8, GID4, GID8, MAEA, MKLN1, RMND5A, RMND5B, RANBP9, RANBP10, WDR26, and YPEL5) and it has been shown to have E3-ligase enzymatic activity. CTLH proteins have been linked to all fundamental biological processes including proliferation, survival, programmed cell death, cell adhesion, and migration. At molecular level, the complex seems to interact and intertwine with key signaling pathways such as the PI3-kinase, WNT, TGFβ, and NFκB, which are key to cancer cell plasticity. As a whole, the CTLH complex is overexpressed in the most prevalent types of cancer and may hold the key to unlock many of the biological secrets that allow cancer cells to thrive in harsh conditions and resist antineoplastic therapy.

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“…In our previous study, we found that RANBP9 was overexpressed in CRC tissues in a small patient cohort. It suppressed CRC cell proliferation both in vitro and in vivo ( 18 ). The aim of this study was to determine the association between RANBP9 expression levels and clinicopathological parameters in an expanded patient cohort, as well as CRC patient prognosis.…”

Section: Introductionmentioning

confidence: 99%

Reduced RANBP9 expression is associated with poor prognosis in colorectal cancer patients

Wu¹,

Li²,

Qin³

2019

Transl Cancer Res TCR

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Background: Colorectal cancer (CRC) is the third most common malignancy worldwide. RANBP9 is a RAN-binding protein that has been reported to be a reliable predictor for prognosis in some human cancers. The mechanism of RANBP9 involvement in CRC carcinogenesis is unknown. This study measured RANBP9 expression levels in CRC to determine its association with clinicopathological parameters.Methods: This study included 228 CRC patients who underwent radical resection. RANBP9 expression was determined using immunohistochemistry. Based on follow-up data, the correlation of RANBP9 expression levels with clinicopathological parameters, including disease free survival (DFS) and overall survival (OS) was evaluated.Results: Reduced RANBP9 expression was correlated with tumor location (P=0.014), vascular invasion (P=0.057) and normal serum carcinoembryonic antigen levels (P=0.001). Patients with reduced RANBP9 expression had a 5-year DFS rate of 63.0% compared to 78.9% for patients with high expression levels of RANBP9 (P=0.015). Subgroup analysis demonstrated that reduced RANBP9 expression was significantly correlated with a worse DFS rate (P=0.037) for patients with left-sided colon cancer. RANBP9 was found to be an independent predictive factor for estimating DFS rate (P=0.029, hazard ratio: 0.580, 95% confidence interval: 0.356-0.946) and OS.Conclusions: RANBP9 expression levels is a potential prognostic factor for estimating CRC survival rates in patients after surgery.

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RANBP9 suppresses tumor proliferation in colorectal cancer

Cited by 6 publications

References 31 publications

RANBP9 as potential therapeutic target in non-small cell lung cancer

RANBP9 as potential therapeutic target in non-small cell lung cancer

The CTLH Complex in Cancer Cell Plasticity

Reduced RANBP9 expression is associated with poor prognosis in colorectal cancer patients

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