&lt;p&gt;Knockdown of SLC35F2 Inhibits the Proliferation and Metastasis of Bladder Cancer Cells&lt;/p&gt;

Chen, Mei; Gào, Xīn; Huang, Denggao; Wang, Shunlan; Zheng, Linlin; Chen, Yinyi; Wen, Xiaohong; Gao, Yuanhui; Cao, Hui; Zhang, Shufang

doi:10.2147/ott.s229332

Cited by 9 publications

(12 citation statements)

References 37 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Our data suggest that SLC35F2 is higher expressed in MIBC as compared with matched NMIBC, indicating that SLC35F2 might be involved in BC progression. This is consistent with observations from Chen et al, who suggested the high SLC35F2 level to be correlated with tumour stage and invasiveness of BC [ 17 ]. Here, we show an increased staining (moderate to strong) of SLC35F2 in single tumour cells and in the cells of the border of solid tumour areas in MIBC compared with matched NMIBC samples, suggesting that these cells might be responsible for the invasiveness and aggressiveness of BC.…”

Section: Discussionsupporting

confidence: 93%

“…The functional role and molecular mechanisms of SLC35F2 in cancer development have not yet been comprehensively investigated. It has been shown that SLC35F2 is highly expressed in NSCLC, PTC, prostate cancer, and BC, and the authors suggest that high SLC35F2 expression is correlated with cancer progression [ 12 , 14 , 16 , 17 ]. Our data suggest that SLC35F2 is higher expressed in MIBC as compared with matched NMIBC, indicating that SLC35F2 might be involved in BC progression.…”

Section: Discussionmentioning

confidence: 99%

“…Moreover, in prostate cancer, SLC35F2 seems to play a role, as it was highly expressed, directly upregulated by the androgen receptor (AR) activation and crucially involved in the sensitivity of prostate cancer cells to YM155 [ 16 ]. One recent publication showed that SLC35F2 is highly expressed in BC tissues and can promote BC progression [ 17 ]. Therefore, understanding the molecular mechanism of SLC35F2 in the progression of cancer might provide new therapeutic opportunities against BC.…”

Section: Introductionmentioning

confidence: 99%

See 2 more Smart Citations

SLC35F2, a Transporter Sporadically Mutated in the Untranslated Region, Promotes Growth, Migration, and Invasion of Bladder Cancer Cells

Kotolloshi

Hölzer

Gajda

et al. 2021

Cells

View full text Add to dashboard Cite

Bladder cancer is a very heterogeneous disease and the molecular mechanisms of carcinogenesis and progression are insufficiently investigated. From the DNA sequencing analysis of matched non-muscle-invasive bladder cancer (NMIBC) and muscle-invasive bladder cancer (MIBC) samples from eight patients, we identified the tumour-associated gene SLC35F2 to be mutated in the 5′ and 3′ untranslated region (UTR). One mutation in 3′UTR increased the luciferase activity reporter, suggesting its influence on the protein expression of SLC35F2. The mRNA level of SLC35F2 was increased in MIBC compared with NMIBC. Furthermore, in immunohistochemical staining, we observed a strong intensity of SLC35F2 in single tumour cells and in the border cells of solid tumour areas with an atypical accumulation around the nucleus, especially in the MIBC. This suggests that SLC35F2 might be highly expressed in aggressive and invasive tumour cells. Moreover, knockdown of SLC35F2 repressed the growth of bladder cancer cells in the monolayer and spheroid model and suppressed migration and invasion of bladder cancer cells. In conclusion, we suggest that SLC35F2 is involved in bladder cancer progression and might provide a new therapeutic approach, for example, by the anti-cancer drug YM155, a cargo of the SLC35F2 transporter.

show abstract

Section: Discussionsupporting

confidence: 93%

Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

See 1 more Smart Citation

SLC35F2, a Transporter Sporadically Mutated in the Untranslated Region, Promotes Growth, Migration, and Invasion of Bladder Cancer Cells

Kotolloshi

Hölzer

Gajda

et al. 2021

Cells

View full text Add to dashboard Cite

show abstract

“…Previous studies have reported that USP32 is expressed at high level in several cancers, include breast cancer 37 , small-cell lung cancer 38 , and gastric carcinomas 39 . In contrast, SLC35F2 is expressed highly in bladder 40 , papillary thyroid 41 , lung 42 , and non-small-cell lung cancer 43 . Based on these variable expression profiles exhibited by USP32 and SLC35F2, the ERAD-mediated proteasomal degradation of SLC35F2 was promoted by USP32.…”

Section: Discussionmentioning

confidence: 94%

USP32 confers cancer cell resistance to YM155 via promoting ER-associated degradation of solute carrier protein SLC35F2

Chandrasekaran¹,

Kaushal²,

Park³

et al. 2021

Theranostics

View full text Add to dashboard Cite

Background: The most commonly preferred chemotherapeutic agents to treat cancers are small-molecule drugs. However, the differential sensitivity of various cancer cells to small molecules and untargeted delivery narrow the range of potential therapeutic applications. The mechanisms responsible for drug resistance in a variety of cancer cells are also largely unknown. Several deubiquitinating enzymes (DUBs) are the main determinants of drug resistance in cancer cells. Methods: We used CRISPR-Cas9 to perform genome-scale knockout of the entire set of genes encoding ubiquitin-specific proteases (USPs) and systematically screened for DUBs resistant to the clinically evaluated anticancer compound YM155. A series of in vitro and in vivo experiments were conducted to reveal the relationship between USP32 and SLC35F2 on YM155-mediated DNA damage in cancer cells. Results: CRISPR-based dual-screening method identified USP32 as a novel DUB that governs resistance for uptake of YM155 by destabilizing protein levels of SLC35F2, a solute-carrier protein essential for the uptake of YM155. The expression of USP32 and SLC35F2 was negatively correlated across a panel of tested cancer cell lines. YM155-resistant cancer cells in particular exhibited elevated expression of USP32 and low expression of SLC35F2. Conclusion: Collectively, our DUB-screening strategy revealed a resistance mechanism governed by USP32 associated with YM155 resistance in breast cancers, one that presents an attractive molecular target for anti-cancer therapies. Targeted genome knockout verified that USP32 is the main determinant of SLC35F2 protein stability in vitro and in vivo , suggesting a novel way to treat tumors resistant to small-molecule drugs.

show abstract

“…However, 20%-25% of NMIBCs can eventually progress to muscle-invasive bladder cancer (MIBC) with lymph node (LN) and distant metastasis, which results in poor prognosis. 3 The overall five-year survival rate of MIBC is less than 50%. 4 Additionally, due to its high recurrence rate, the therapeutic cost is prohibitive for most BCa patients.…”

Section: Introductionmentioning

confidence: 99%

RPN2 Predicts Poor Prognosis and Promotes Bladder Cancer Growth and Metastasis via the PI3K-Akt Pathway

Han

Chen

et al. 2021

OTT

View full text Add to dashboard Cite

Background Ribophorin II (RPN2) is a highly conserved glycoprotein involved in the N-linked glycosylation of multiple proteins. RPN2 was reported to be associated with malignant phenotype in several tumors. However, the function of RPN2 in bladder cancer (BCa) remains unclear. Methods Expression of RPN2 in BCa and adjacent tissues was compared by bioinformatics analysis, immunohistochemistry, and Western blotting. qRT-PCR was performed to explore the correlation between RPN2 expression and various clinical features in 38 patients. We assessed the effects of RPN2 on the biological activity of BCa both in vitro and in vivo, and explored its potential mechanisms based on gene set enrichment analysis (GSEA). Results We found that RPN2 was highly expressed in human BCa compared with normal adjacent tissues. There was a significant positive correlation between higher RPN2 mRNA levels and tumor T stage, lymph node (LN) metastasis and the degree of pathological differentiation in 38 patients with BCa. We further demonstrated that RPN2 silencing inhibited the growth and metastasis of BCa both in vitro and in vivo. Western blotting revealed that RPN2 knockdown suppressed epithelial-mesenchymal transition (EMT) and inhibited the PI3K-Akt pathway. Conclusion These data suggest that RPN2 functions as an oncogene to promote tumor development and is a promising prognostic factor and therapeutic target in BCa.

show abstract

<p>Knockdown of SLC35F2 Inhibits the Proliferation and Metastasis of Bladder Cancer Cells</p>

Cited by 9 publications

References 37 publications

SLC35F2, a Transporter Sporadically Mutated in the Untranslated Region, Promotes Growth, Migration, and Invasion of Bladder Cancer Cells

SLC35F2, a Transporter Sporadically Mutated in the Untranslated Region, Promotes Growth, Migration, and Invasion of Bladder Cancer Cells

USP32 confers cancer cell resistance to YM155 via promoting ER-associated degradation of solute carrier protein SLC35F2

RPN2 Predicts Poor Prognosis and Promotes Bladder Cancer Growth and Metastasis via the PI3K-Akt Pathway

Contact Info

Product

Resources

About