DC - SIGNR by influencing the lncRNA HNRNPKP2 upregulates the expression of CXCR4 in gastric cancer liver metastasis

Zhang, Yu; Zhang, Qianshi; Zhang, Mengyang; Yuan, Ming; Wang, Zhaohui; Zhang, Jingbo; Xu, Zhou; Zhang, Yinan; Lin, Fang; Na, Heya; Ren, Shuo; Zuo, Yongchun

doi:10.1186/s12943-017-0639-2

Cited by 38 publications

(36 citation statements)

References 43 publications

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“…For example, the binding of EZH2 to lncRNA (AGAP2‐AS1) in GC promotes the invasion of GC cells via binding enhancers of zeste homolog 2 (EZH2) while suppressing E‐cadherin . HNRNPKP2 contributes to the progression of GC, which serves as an indicator of poor prognosis . Additionally, the elevated AK023391 is related to poor prognosis of GC .…”

Section: Discussionmentioning

confidence: 99%

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LncRNA LOC285194 modulates gastric carcinoma progression through activating Wnt/β‐catenin signaling pathway

Zhong

Wang

et al. 2020

Cancer Medicine

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Emerging evidences have revealed long noncoding RNAs (lncRNAs’) critical roles in diverse human carcinoma. Among these cancers, lncRNA LOC285194 has been extensively investigated in several types of carcinomas in the recent years. Nevertheless, the biological function, clinical relevance, and the influence of LOC285194 in gastric cancer (GC) are not fully understood. The present study aims to explore the biological function of LOC285194 in the progression and development of GC. First, LOC285194 expressions were detected in GC tissues and cell lines. The functional role of LOC285194 in GC was evaluated both in vitro and in vivo. Our data found that LOC285194 was lowly expressed both in human GC tissues and GC cell lines compared with corresponding normal controls. Moreover, LOC285194 was mitigated by transfection with LV‐LOC285194 in both HGC‐27 and MKN45 cell lines. Silencing of LOC285194 remarkably induced GC cell livability and cell proliferation. On the contrary, the LOC285194 overexpression suppressed MKN45 and HGC‐27 cell proliferation and promoted cell apoptosis. Additionally, silencing of LOC285194 increased the ability of colony formation, cell migration, and invasive capacities, together with blocking the apoptotic rates of GC cells. Correspondently, LOC285194 overexpression exerted the opposite effects. Mechanistically, silencing of LOC285194 promoted GC progression via inducing Wnt signaling activity. Moreover, in vivo xenografts nude mice model results showed that LOC285194 inhibited GC progression through targeting Wnt signaling. Taken together, LOC285194 is associated with GC progression by regulating the Wnt signaling transduction, potentiating LOC285194's promising role as a novel treatment biomarker in GC.

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Section: Discussionmentioning

confidence: 99%

“…12 HNRNPKP2 contributes to the progression of GC, which serves as an indicator of poor prognosis. 13 Additionally, the elevated AK023391 is related to poor prognosis of GC. 14 Here in our investigation, the biological role of LOC285194 in GC was elucidated.…”

Section: Discussionmentioning

confidence: 99%

LncRNA LOC285194 modulates gastric carcinoma progression through activating Wnt/β‐catenin signaling pathway

Zhong

Wang

et al. 2020

Cancer Medicine

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“…Similarly, CLEC18B expression was significantly altered in glioblastoma multiforme tissue, and was identified as an independent predictor of patient survival (10). Additionally, it has been demonstrated that selectin influences the progression of numerous cancer types, including colon carcinoma (11,12) and gastric cancer (13). Coupland et al (14) discovered that P-selectin promoted the lung metastasis of breast cancer and melanoma in vivo.…”

Section: High Expression Levels Of Clec4m Indicate Poor Prognosis In mentioning

confidence: 99%

“…For example, CLEC4M is associated with poor prognosis in patients with colon cancer, and it is involved in the adhesion, migration, invasion and liver metastasis of colon cancer cells (21). Furthermore, CLEC4M exerts these biological functions through the signal transducer and activator of transcription 5/long non-coding RNA Heterogeneous Nuclear Ribonucleoprotein K Pseudogene 2/ C-X-C chemokine receptor type 4 axis (13). Although CLEC4M has been examined in several malignant tumor types, to our knowledge, the clinical significance of CLEC4M has never been investigated in HCC so far.…”

Section: High Expression Levels Of Clec4m Indicate Poor Prognosis In mentioning

confidence: 99%

High expression levels of CLEC4M indicate poor prognosis in patients with hepatocellular carcinoma

Luo

Zhao

et al. 2020

Oncol Lett

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The identification of novel and accurate biomarkers is important to improve the prognosis of patients with hepatocellular carcinoma (HCC). C-Type lectin domain family 4 member M (CLEC4M) is involved in the progression of numerous cancer types. However, the clinical significance of CLEC4M in HCC is yet to be elucidated. The aim of the present study is to evaluate the involvement of CLEC4M in HCC progression. The expression level of CLEC4M was determined in tumor, and their corresponding adjacent non-tumor tissues derived from 88 patients with HCC, using immunohistochemistry, western blot and reverse transcription-quantitative PCR. The correlation between CLEC4M expression and certain clinicopathological characteristics was retrospectively analyzed. The results suggested that CLEC4M was specifically labeled in sinusoidal endothelial cells, in both HCC and non-tumor tissues. Moreover, the expression of CLEC4M in tumor tissues was significantly lower than that in non-tumor tissues (P<0.0001), which indicated its potential as a biomarker of the development of HCC. Subsequently, correlation analysis suggested that the relatively higher CLEC4M expression in HCC tissues was significantly associated with increased microvascular invasion (P= 0.008), larger tumor size (P= 0.018), absence of tumor encapsulation (P<0.0001) and lower tumor differentiation (P= 0.019). Notably, patients with high CLEC4M expression levels in their tumor tissues experienced more frequent recurrence and shorter overall survival (OS) times compared with the low-expression group. Furthermore, CLEC4M expression in tumor tissues was identified as an independent and significant risk factor for recurrence-free survival and OS. The results of the present study suggest that CLEC4M may be a valuable biomarker for the prognosis of the patients with HCC, postoperatively.

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“…Abnormal expression and regulation of lncRNAs were involved in oncogenesis and development, including GC. PVT1, HNRNPKP2, HOXA11-AS and many other lncRNAs can affect the malignant phenotype of GC cells at transcriptional and post-transcriptional levels [7][8][9]. In 2015, lncRNA Downregulated RNA in cancer (DRAIC) was firstly reported as a target gene of FOXA1 and NKX3-1 to inhibit the ability of transition from an androgendependent (AD) to a castration-resistance state, epithelial-mesenchymal transition (EMT) and metastasis of prostate cancer cells, and TCGA database analysis showed that its expression was closely related to the survival rate of patients with malignant tumors such as GC, lung cancer and hepatocellular carcinoma [10,11].…”

Section: Introductionmentioning

confidence: 99%

LncRNA DRAIC inhibits proliferation and metastasis of gastric cancer cells through interfering with NFRKB deubiquitination mediated by UCHL5

Zhang

Kuang

et al. 2020

Cell Mol Biol Lett

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Background: Long non-coding RNA (lncRNA) as a widespread and pivotal epigenetic molecule participates in the occurrence and progression of malignant tumors. DRAIC, a kind of lncRNA whose coding gene location is on 15q23 chromatin, has been found to be weakly expressed in a variety of malignant tumors and acts as a suppressor, but its characteristics and role in gastric cancer (GC) remain to be elucidated. Methods: Sixty-seven primary GC tissues and paired paracancerous normal tissues were collected. Bioinformatics is used to predict the interaction molecules of DRAIC. DRAIC and NFRKB were overexpressed or interfered exogenously in GC cells by lentivirus or transient transfection. Quantitative real-time PCR (qPCR) and western blotting were used to evaluate the expression of DRAIC, UCHL5 and NFRKB. The combinations of DRAIC and NFRKB or UCHL5 and NFRKB were verified by RNA-IP and Co-IP assays. Ubiquitination-IP and the treatment of MG132 and CHX were used to detect the ubiquitylation level of NFRKB. The CCK-8 and transwell invasion and migration assays measured the proliferation, migration and invasion of GC cells. Results: DRAIC is down-regulated in GC tissues and cell lines while its potential interacting molecules UCHL5 and NFRKB are up-regulated, and DRAIC is positively correlated with NFRKB protein instead of mRNA. Lower DRAIC and higher UCHL5 and NFRKB indicated advanced progression of GC patients. DRAIC could increase NFRKB protein significantly instead of NFRKB mRNA and UCHL5, and bind to UCHL5. DRAIC combined with UCHL5 and attenuated binding of UCHL5 and NFRKB, meanwhile promoting the degradation of NFRKB via ubiquitination, and then inhibited the proliferation and metastasis of GC cells, which can be rescued by oeNFRKB. Conclusion: DRAIC suppresses GC proliferation and metastasis via interfering with the combination of UCHL5 and NFRKB and mediating ubiquitination degradation.

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DC - SIGNR by influencing the lncRNA HNRNPKP2 upregulates the expression of CXCR4 in gastric cancer liver metastasis

Cited by 38 publications

References 43 publications

LncRNA LOC285194 modulates gastric carcinoma progression through activating Wnt/β‐catenin signaling pathway

LncRNA LOC285194 modulates gastric carcinoma progression through activating Wnt/β‐catenin signaling pathway

High expression levels of CLEC4M indicate poor prognosis in patients with hepatocellular carcinoma

LncRNA DRAIC inhibits proliferation and metastasis of gastric cancer cells through interfering with NFRKB deubiquitination mediated by UCHL5

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