PCAT6 mediates cellular biological functions in gastrointestinal stromal tumor via upregulation of PRDX5 and activation of Wnt pathway

Bai, Fangyun; Zhang, Na; Fang, Wei; He, Xiangyi; Zheng, Yan; Gu, Danan

doi:10.1002/mc.23199

Cited by 14 publications

(18 citation statements)

References 20 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Previously, prostate cancer-associated transcript 6 (PCAT6) has been identified as an lncRNA involved in the regulation of lung cancer progression (14). Subsequently, several studies have highlighted the abnormal expression of lncRNA PCAT6 in various malignant tumors, including gastrointestinal stromal tumor, colon cancer and osteosarcoma, suggesting that PCAT6 may play an essential role in tumor progression (15)(16)(17). Although the oncogenic roles of PCAT6 have been demonstrated in several tumors,…”

Section: Introductionmentioning

confidence: 99%

lncRNA PCAT6 facilitates cell proliferation and invasion via regulating the miR‑326/hnRNPA2B1 axis in liver cancer

et al. 2021

View full text Add to dashboard Cite

Liver cancer is one of the most common malignant human tumors with the highest morbidity and mortality rates of all cancer types in China. Evidence suggests that long non-coding RNA prostate cancer-associated transcript 6 (PCAT6) plays an essential role in tumor progression. However, the roles and mechanism of PCAT6 in liver cancer remain unclear. The present study showed that the expression of PCAT6 and heterogeneous nuclear ribonucleoprotein A2B1 (hnRNPA2B1) was upregulated in liver cancer tissues compared with non-cancerous tissues and were associated with poor overall survival time, whereas microRNA (miR)-326 expression was downregulated. Moreover, knockdown of PCAT6 significantly inhibited the proliferation and invasion of liver cancer cells in vitro and in vivo. A dual-luciferase reporter gene assay demonstrated that PCAT6 could bind to miR-326 and that hnRNPA2B1 was a direct target gene of miR-326. Mechanistically, silenced PCAT6 suppressed the malignant phenotype of liver cancer cells through upregulating the inhibitory effect of miR-326 on hnRNPA2B1 expression. Taken together, these data demonstrated that knockdown of PCAT6 inhibited liver cancer progression through regulation of the miR-326/hnRNPA2B1 axis, suggesting that PCAT6 functions as an oncogene and may be a useful biomarker for the future diagnosis and treatment of liver cancer.

show abstract

Section: Introductionmentioning

confidence: 99%

lncRNA PCAT6 facilitates cell proliferation and invasion via regulating the miR‑326/hnRNPA2B1 axis in liver cancer

et al. 2021

View full text Add to dashboard Cite

show abstract

“…lncRNA PCAT6 is a lncRNA that has been reported to be upregulated in osteosarcoma and colorectal cancer (26,27) and has emerged as a critical regulator in tumorigenesis and cancer progression. For example, Bai et al (28) have demonstrated that PCAT6 promotes gastrointestinal stromal tumor cell proliferation and stemness, but inhibits apoptosis through the ceRNA mechanism and the activation of the Wnt signaling pathway. Ma et al (14) have reported that PCAT6 facilitates the proliferation, migration and cisplatin resistance of cervical cancer cells and impedes their apoptosis via the PCAT6/miR-543/zinc finger E-box-binding homeobox 1 axis.…”

Section: Discussionmentioning

confidence: 99%

Long non‑coding RNA PCAT6 regulates bladder cancer progression via the microRNA‑143‑3p/PDIA6 axis

2021

View full text Add to dashboard Cite

Although long non-coding (lnc)RNAs have been reported to be involved in the pathological development of bladder cancer, the functions of lncRNA prostate cancer-associated transcript 6 (PCAT6) and its underlying mechanism of action in bladder cancer remain unknown. The present study aimed to investigate the effect of PCAT6 in bladder cancer progression and explore its potential application as a novel treatment target. The expression of PCAT6 and miR-143-3p in bladder cancer tissues, adjacent normal tissues and cell lines was measured using reverse transcription-quantitative PCR. Fluorescence in situ hybridization assay was used to detect the subcellular localization of PCAT6. MTT, EdU, Transwell and wound healing assays were conducted to assess the biological function of PCAT6 on cell proliferation, migration and invasion. Putative binding sites between miR-143-3p and PCAT6 or PDIA6 were predicted using starBase, Lncbase and TargetScan analyzes. Dual-luciferase reporter assay was also used to confirm the potential binding between PCAT6 and miR-143-3p. RNA immunoprecipitation assay was performed to verify the possible interaction between PCAT6 and miR-143-3p. Western blotting was used to measure the expression of PDIA6. The results demonstrated that the expression levels of PCAT6 were upregulated in bladder cancer tissues relative to those in adjacent normal bladder tissues. Knockdown of PCAT6 served a role in suppressing the proliferation, migration and invasion of T24T and EJ bladder cancer cells. PCAT6 knockdown contributed to a reduction of PDIA6 expression at the mRNA and protein levels compared with that in negative control-transfected cells, whilst the miR-143-3p inhibitor partially mitigated this reduction effect. In addition, rescue experiments revealed that the miR-143-3p inhibitors reversed the effects of PCAT6 silencing on the malignant phenotypes of bladder cancer. Collectively, the results of the present study demonstrated that PCAT6 may serve an oncogenic role in bladder cancer via the miR-143-3p/PDIA6 axis. These results may provide a potential therapeutic target for the treatment of bladder cancer.

show abstract

“…Further, in silico pathway and network analyses implicated the hypoxia-inducible factor 1 pathway as a mediator of imatinib resistance. The role of the lncRNA prostate cancer-associated transcript 6 (PCAT6) was examined by Bai et al [131]. First, PCAT6 was found to be upregulated in GIST in comparison with adjacent non-cancerous tissue.…”

Section: Additional Non-coding Rnas In Gastrointestinal Stromal Tumorsmentioning

confidence: 99%

“…Finally, miRNAs associated with imatinib resistance [30,110,114,115,[117][118][119] may be used to signal evolving imatinib resistance enabling early clinical intervention. Interestingly, lncRNAs have also been identified that could be used for diagnostic purposes [129,131,133] or are specifically linked to high-risk/advanced GIST [108,122,123,125,128] and imatinib resistance [126,127,130]. However, more research is necessary to select the miRNA classifiers that are most promising for validation in prospective clinical studies.…”

Section: Biomarkersmentioning

confidence: 99%

“…Alternative targets with therapeutic potential are PDGFRA , reported to be targeted by miR-34a [ 97 ], PTEN [ 100 ], BIRC5 [ 93 ] and APOC2 [ 101 ]. The lncRNAs HOTAIR [ 108 , 122 , 123 ], AOC4P [ 125 ] and PCAT6 [ 131 ] are also amenable for therapeutic modulation. In principle, one could restore expression of non-coding RNAs that display reduced levels in cancer using mimics.…”

Section: Therapeutic Potential Of Non-coding Rnasmentioning

confidence: 99%

See 1 more Smart Citation

Non-Coding RNAs, a Novel Paradigm for the Management of Gastrointestinal Stromal Tumors

Amirnasr

Sleijfer

Wiemer

2020

IJMS

View full text Add to dashboard Cite

Gastrointestinal stromal tumors (GISTs) are the most common mesenchymal malignancies found in the gastrointestinal tract. At a molecular level, most GISTs are characterized by gain-of-function mutations in V-Kit Hardy–Zuckerman 4 Feline Sarcoma Viral Oncogene Homolog (KIT) and Platelet Derived Growth Factor Receptor Alpha (PDGFRA), leading to constitutive activated signaling through these receptor tyrosine kinases, which drive GIST pathogenesis. In addition to surgery, treatment with the tyrosine kinase inhibitor imatinib forms the mainstay of GIST treatment, particularly in the advanced setting. Nevertheless, the majority of GISTs develop imatinib resistance. Biomarkers that indicate metastasis, drug resistance and disease progression early on could be of great clinical value. Likewise, novel treatment strategies that overcome resistance mechanisms are equally needed. Non-coding RNAs, particularly microRNAs, can be employed as diagnostic, prognostic or predictive biomarkers and have therapeutic potential. Here we review which non-coding RNAs are deregulated in GISTs, whether they can be linked to specific clinicopathological features and discuss how they can be used to improve the clinical management of GISTs.

show abstract

PCAT6 mediates cellular biological functions in gastrointestinal stromal tumor via upregulation of PRDX5 and activation of Wnt pathway

Cited by 14 publications

References 20 publications

lncRNA PCAT6 facilitates cell proliferation and invasion via regulating the miR‑326/hnRNPA2B1 axis in liver cancer

lncRNA PCAT6 facilitates cell proliferation and invasion via regulating the miR‑326/hnRNPA2B1 axis in liver cancer

Long non‑coding RNA PCAT6 regulates bladder cancer progression via the microRNA‑143‑3p/PDIA6 axis

Non-Coding RNAs, a Novel Paradigm for the Management of Gastrointestinal Stromal Tumors

Contact Info

Product

Resources

About