Long Noncoding Competing Endogenous RNA Networks in Pancreatic Cancer

Xiong, Guangbing; Pan, Shutao; Jin, Junyang; Wang, Xiaoxiang; He, Ruizhi; Peng, Feng; Xu, Li; Wang, Min; Zheng, Jie; Zhu, Feng; Qin, Renyi

doi:10.3389/fonc.2021.765216

Cited by 11 publications

(6 citation statements)

References 276 publications

(432 reference statements)

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“…Previous literature has shown that expression of lncRNAs is altered in many malignancies including pancreatic cancer. 27 It has been reported that H19 expression is high in pancreatic cancer tissues. It has also been shown that H19 expression is higher in metastasized tumors.…”

Section: Discussionmentioning

confidence: 99%

İnsan Pankreas Kanserinde Borik Asit Uygulaması ile Bazı IncRNA’ların ve İnvazyonun Baskılanması

Eroğlu

2023

Online Türk Sağlık Bilimleri Dergisi

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Amaç: Borik asidin bazı lncRNA'lar ve invazyon üzerine etkisinin PANC-1 ve MIA PaCa-2 pankreas kanseri hücrelerinde araştırılması amaçlanmıştır. Materyal ve Metot: Borik asitin hücre canlılığı ve invazyon üzerine etkileri sırası ile XTT testi ve invazyon kuyucukları kullanılarak araştırılmıştır. TCGA verileri kullanılarak pankreas kanserinde lncRNA H19 ve UCA1 ifadeleri değerlendirilmiştir. Bu lncRNA’ların ve invazyon genlerinin ifadeleri üzerine etkileri qRT-PZR ile belirlenmiştir. Bulgular: PANC-1 hücrelerinde borik asitin IC50 dozu 14248,8 µM, MIA PaCa-2 de 15707,5 µM olarak hesaplanmıştır. TCGA verileri H19 ve UCA1 ifadelerinin pankreas kanserinde yüksek olduğunu göstermiştir. Borik asit muamelesi ile H19 ve UCA1 lncRNA seviyeleri azalmıştır. Ayrıca borik asit iki hücre hattında CDH1 ve TIMP1 ifadesini arttırmıştır. CDH2 ifadesi ise baskılanmıştır. Borik asit PANC-1 hücrelerinde TIMP2, MIA PaCa-2 hücrelerinde TIMP3 ifadesini arttırmıştır. İnvazyon testinde borik asit her iki hücrede invazyonu anlamlı derecede baskılanmıştır. Sonuç: Borik asit pankreas kanseri hücrelerinde ifadesinin yüksek olduğu görülen H19 ve UCA1 ifadelerini baskılamıştır. Ayrıca invazyonda önemli olan genlerin ifadelerini değiştirerek anti-invazif etki göstermiştir.

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Section: Discussionmentioning

confidence: 99%

İnsan Pankreas Kanserinde Borik Asit Uygulaması ile Bazı IncRNA’ların ve İnvazyonun Baskılanması

Eroğlu

2023

Online Türk Sağlık Bilimleri Dergisi

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“…On one hand, lncRNAs act as miRNA sponges and competitive endogenous RNAs (ceRNAs) of miRNAs to hinder the binding of miRNAs to target genes. 21 LncRNA HAGLR sponges miR-338-3p to accelerate 5-Fu resistance in gastric cancer via targeting the LDHA-glycolysis pathway. 22 The ceRNA network formed by lncRNA–miRNA–mRNA plays a crucial part in several cancers including gastric cancer.…”

Section: Discussionmentioning

confidence: 99%

LINC01232 Promotes Metastasis and EMT by Regulating miR-506-5p/PAK1 Axis in Gastric Cancer

Chen¹,

Liao²,

Xu³

et al. 2022

CMAR

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Background Long non-coding RNA LINC01232 plays an important role in the progression of metastasis in several cancers. However, the function of LINC01232 in gastric cancer is limited. Authors aimed to investigate the role and mechanism of LINC01232 in the metastasis of gastric cancer. Methods The expression levels and correlation of LINC01232, miR-506-5p, and PAK1 were analyzed by GEPIA or ENCORI, and the abundance of LINC01232 and miR-506-5p was measured in tissues and cells via qRT-PCR, the location of LINC01232 in gastric cells was analyzed by nuclear and cytoplasmic fractionation, while the protein levels of PAK1, E-cadherin and vimentin were additionally quantified by Western blotting. Interactions between LINC01232, miR-506-5p, and PAK1 were detected through luciferase reporter assays, qRT-PCR and Western blotting. Cellular viability was evaluated through CCK8 assays, migration ability was measured by transwell assays, invasion ability was tested by wound healing experiment. Results LINC01232 was overexpressed in gastric cancer tissues and cells, and mainly located in nucleus. The inhibition of LINC01232 could suppress migration, invasion and EMT of gastric cancer cells. MiR-506-5p was downregulated in gastric cancer tissues and cells. LINC01232 sponged miR-506-5p to accelerate migration and EMT. PAK1 was certified to be a target of miR-506-5p, inhibition of PAK1 could interrupt LINC01232 overexpression-induced migration of gastric cancer cells. Conclusion The LINC01232/miR-506-5p/PAK1 axis promotes metastasis of gastric cancer cells.

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“…This phenomenon leads to the deregulation of miRNA function with several effects on the genome. Modulation of PVT1 that takes part in pancreatic carcinogenesis and chemoresistance to gemcitabine, is also considered a potent druggable target, while it is proven that the knockdown of PVT1could suppress the autophagy mechanism and limit the chemoresistance to gemcitabine by miR-143/HIF-1α/VMP1 axis [ 114 , 115 , 116 , 117 , 118 , 119 , 120 ]. Another example of miRNA-related autophagy inhibition that suppresses PDAC grow this mediated by miR-7 and miR-372 [ 121 , 122 ].…”

Section: The Interplay Of Autophagy and Mirnas In Pdacmentioning

confidence: 99%

The Emerging Role of MicroRNAs and Autophagy Mechanism in Pancreatic Cancer Progression: Future Therapeutic Approaches

Koustas

Trifylli²,

Sarantis

et al. 2022

Genes

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Pancreatic cancer constitutes the fourth most frequent cause of death due to malignancy in the US. Despite the new therapeutic modalities, the management of pancreatic ductal adenocarcinoma (PDAC) is considered a difficult task for clinicians due to the fact that is usually diagnosed in already advanced stages and it is relatively resistant to the current chemotherapeutic agents. The molecular background analysis of pancreatic malignant tumors, which includes various epigenetic and genetic alterations, opens new horizons for the development of novel diagnostic and therapeutic strategies. The interplay between miRNAs, autophagy pathway, and pancreatic carcinogenesis is in the spotlight of the current research. There is strong evidence that miRNAs take part in carcinogenesis either as tumor inhibitors that combat the oncogene expression or as promoters (oncomiRs) by acting as oncogenes by interfering with various cell functions such as proliferation, programmed cell death, and metabolic and signaling pathways. Deregulation of the expression levels of various miRNAs is closely associated with tumor growth, progression, and dissemination, as well as low sensitivity to chemotherapeutic agents. Similarly, autophagy despite constituting a pivotal homeostatic mechanism for cell survival has a binary role in PDAC, either as an inhibitor or promoter of carcinogenesis. The emerging role of miRNAs in autophagy gets a great deal of attention as it opens new opportunities for the development of novel therapeutic strategies for the management of this aggressive and chemoresistant malignancy. In this review, we will shed light on the interplay between miRNAs and the autophagy mechanism for pancreatic cancer development and progression.

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Long Noncoding Competing Endogenous RNA Networks in Pancreatic Cancer

Cited by 11 publications

References 276 publications

İnsan Pankreas Kanserinde Borik Asit Uygulaması ile Bazı IncRNA’ların ve İnvazyonun Baskılanması

İnsan Pankreas Kanserinde Borik Asit Uygulaması ile Bazı IncRNA’ların ve İnvazyonun Baskılanması

LINC01232 Promotes Metastasis and EMT by Regulating miR-506-5p/PAK1 Axis in Gastric Cancer

The Emerging Role of MicroRNAs and Autophagy Mechanism in Pancreatic Cancer Progression: Future Therapeutic Approaches

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