scholarly journals The expression pattern of long non-coding RNA PVT1 in tumor tissues and in extracellular vesicles of colorectal cancer correlates with cancer progression

Tumor Biology ◽  
2017 ◽  
Vol 39 (4) ◽  
pp. 101042831769912 ◽  
Author(s):  
Kai Guo ◽  
Jie Yao ◽  
Qiang Yu ◽  
Zijian Li ◽  
Hu Huang ◽  
...  
Keyword(s):  
Colorectal Cancer ◽  
Expression Pattern ◽  
Extracellular Vesicles ◽  
Cancer Progression ◽  
Non Coding Rna ◽  
Tumor Tissues ◽  
Long Non Coding Rna

scholarly journals Long non-coding RNA AGER-1 inhibits colorectal cancer progression through sponging miR-182

2020 ◽  
Vol 35 (1) ◽  
pp. 10-18 ◽  
Author(s):  
Mingzhu Lin ◽  
Yinyan Li ◽  
Jianfeng Xian ◽  
Jinbin Chen ◽  
Yingyi Feng ◽  
...  
Keyword(s):  
Colorectal Cancer ◽  
Cancer Progression ◽  
Ectopic Expression ◽  
Tumor Development ◽  
Vital Role ◽  
Normal Tissues ◽  
Non Coding Rna ◽  
Colorectal Cancer Progression ◽  
And Migration ◽  
Long Non Coding Rna

Objective: Abundant evidence has illustrated that long non-coding RNA (lncRNA) plays a vital role in the regulation of tumor development and progression. Ectopic expression of a novel lncRNA, termed lnc-AGER-1, has been discovered in cancers, and this lncRNA was reported to exert an anti-tumor effect. However, its biological mechanism remains unelucidated in colorectal cancer. Methods: A total of 159 paired colorectal cancer specimens and adjacent tissues was applied to detect the expression of lnc-AGER-1 by the quantitative Real-time PCR (qRT-PCR), and a series of functional assays was executed to uncover the role of this lncRNA on colorectal cancer. Results: We found that the expression of lnc-AGER-1 in the tumor tissues was significantly down-regulated, while compared with adjacent normal tissues (0.0115 ± 0.0718 vs. 0.0347 ± 0.157; P < 0.0001). Also, lnc-AGER-1 was observably associated with clinical T status (r = −0.184, P = 0.024). Patients with advanced T status exerted a significantly lower level of lnc-AGER-1 than those with early T status (20.0% vs. 40.7%, P = 0.021). Over-expression of lnc-AGER-1 inhibited cell proliferation and migration efficiency, and induced cell cycle arrest at the G0/G1 phase, and promoted cell apoptosis. Further research proved that lnc-AGER-1 altered the expression of its neighbor gene, AGER, through acting as a competing endogenous RNA for miR-182 in colorectal cancer. Conclusion: lnc-AGER-1 has a suppressive role in colorectal cancer development via modulating AGER, which may serve as a target for colorectal cancer diagnosis and treatment.

scholarly journals Long non-coding RNA RAMS11 promotes metastatic colorectal cancer progression

2020 ◽  
Vol 11 (1) ◽  
Author(s):  
Jessica M. Silva-Fisher ◽  
Ha X. Dang ◽  
Nicole M. White ◽  
Matthew S. Strand ◽  
Bradley A. Krasnick ◽  
...  
Keyword(s):  
Colorectal Cancer ◽  
Metastatic Colorectal Cancer ◽  
Cancer Progression ◽  
Non Coding Rna ◽  
Colorectal Cancer Progression ◽  
Long Non Coding Rna

scholarly journals ANRIL promotes chemoresistance via disturbing expression of ABCC1 by regulating the expression of Let-7a in colorectal cancer

2018 ◽  
Vol 38 (6) ◽  
Author(s):  
Zhen Zhang ◽  
Lifeng Feng ◽  
Pengfei Liu ◽  
Wei Duan
Keyword(s):  
Colorectal Cancer ◽  
Cancer Progression ◽  
Clinical Prognosis ◽  
Normal Tissues ◽  
Kaplan Meier ◽  
Non Coding Rna ◽  
Tumor Tissues ◽  
Oncogenic Gene ◽  
Poor Clinical Prognosis

Increasing evidence indicates that long non-coding RNAs (lncRNAs) antisense non-coding RNA in the INK4 locus (ANRIL) has been involved in various diseases and promotes tumorigenesis and cancer progression as an oncogenic gene. However, the effect of ANRIL on chemoresistance remains still unknown in colorectal cancer (CRC). Here, we investigated ANRIL expression in 63 cases of colorectal cancer specimens and matched normal tissues. Results revealed that ANRIL was up-regulated in tumor tissues samples from patients with CRC and CRC cell lines. Increased ANRIL expression in CRC was associated with poor clinical prognosis. Kaplan–Meier analysis showed that ANRIL was associated with overall survival of patients with colorectal cancer, and patients with high ANRIL expression tended to have unfavorable outcome. In vitro experiments revealed that ANRIL knockdown significantly inhibited CRC cell proliferation, improved the sensitivity of chemotherapy and promoted apoptosis. Further functional assays indicated that ANRIL overexpression significantly promoted cell chemoresistance by regulating ATP-binding cassette subfamily C member 1 through binding Let-7a. Taken together, our study demonstrates that ANRIL could act as a functional oncogene in CRC, as well as a potential therapeutic target to inhibit CRC chemoresistance.

scholarly journals The long non-coding RNA CYTOR drives colorectal cancer progression by interacting with NCL and Sam68

2018 ◽  
Vol 17 (1) ◽  
Author(s):  
Xue Wang ◽  
Hongfei Yu ◽  
Wenjie Sun ◽  
Jianlu Kong ◽  
Lei Zhang ◽  
...  
Keyword(s):  
Colorectal Cancer ◽  
Cancer Progression ◽  
Non Coding Rna ◽  
Colorectal Cancer Progression ◽  
Long Non Coding Rna

scholarly journals Genome-wide analysis of long non-coding RNA expression and function in colorectal cancer

Tumor Biology ◽  
2017 ◽  
Vol 39 (5) ◽  
pp. 101042831770365 ◽  
Author(s):  
Fangyuan Jing ◽  
Huicheng Jin ◽  
Yingying Mao ◽  
Yingjun Li ◽  
Ye Ding ◽  
...  
Keyword(s):  
Colorectal Cancer ◽  
Expression Profile ◽  
Colorectal Carcinogenesis ◽  
Rna Expression ◽  
Rna Transcripts ◽  
Non Coding Rna ◽  
Tumor Tissues ◽  
Non Coding Rnas ◽  
Long Non Coding Rna

Long non-coding RNAs (lncRNAs) are widely transcribed in the genome, but their expression profile and roles in colorectal cancer are not well understood. The aim of this study was to investigate the long non-coding RNA expression profile in colorectal cancer and look for potential diagnostic biomarkers of colorectal cancer. Long non-coding RNA microarray was applied to investigate the global long non-coding RNA expression profile in colorectal cancer. Gene ontology and Kyoto Encyclopedia of Genes and Genomes pathway analyses were performed using standard enrichment computational methods. The expression levels of selected long non-coding RNAs were validated by quantitative reverse transcription polymerase chain reaction. The relationship between long non-coding RNA expression levels and clinicopathological characteristics of colorectal cancer patients was assessed. Coexpression analyses were carried out to find the coexpressed genes of differentially expressed long non-coding RNAs, followed by gene ontology analysis to predict the possible role of the selected long non-coding RNAs in colorectal carcinogenesis. In this study, a total of 1596 long non-coding RNA transcripts and 1866 messenger RNA transcripts were dysregulated in tumor tissues compared with paired normal tissues. The top upregulated long non-coding RNAs in tumor tissues were CCAT1, UCA1, RP5-881L22.5, NOS2P3, and BC005081 and the top downregulated long non-coding RNAs were AK055386, AC078941.1, RP4-800J21.3, RP11-628E19.3, and RP11-384P7.7. Long non-coding RNA UCA1 was significantly upregulated in colon cancer, and AK055386 was significantly downregulated in tumor with dimension <5 cm. Functional prediction analyses showed that both the long non-coding RNAs coexpress with cell cycle related messenger RNAs. The current long non-coding RNA study provided novel insights into expression profile in colorectal cancer and predicted the potential roles of long non-coding RNAs in colorectal carcinogenesis. Among the dysregulated long non-coding RNAs, UCA1 was found to be associated with anatomic site, and AK055386 was found associated with tumor size. Further functional investigations into the molecular mechanisms are warranted to clarify the role of long non-coding RNA in colorectal carcinogenesis.

scholarly journals Long Non-Coding RNA SNHG16 Activates USP22 Expression to Promote Colorectal Cancer Progression by Sponging miR-132-3p

2020 ◽  
Vol Volume 13 ◽  
pp. 4283-4294
Author(s):  
Xiaowen He ◽  
Jun Ma ◽  
Mingming Zhang ◽  
Jianhua Cui ◽  
Hao Yang
Keyword(s):  
Colorectal Cancer ◽  
Cancer Progression ◽  
Non Coding Rna ◽  
Colorectal Cancer Progression ◽  
Long Non Coding Rna

scholarly journals Extracellular Vesicles in Bone Metastasis: Key Players in the Tumor Microenvironment and Promising Therapeutic Targets

2020 ◽  
Vol 21 (18) ◽  
pp. 6680 ◽  
Author(s):  
Takaaki Tamura ◽  
Yusuke Yoshioka ◽  
Shinichi Sakamoto ◽  
Tomohiko Ichikawa ◽  
Takahiro Ochiya
Keyword(s):  
Bone Metastasis ◽  
Tumor Microenvironment ◽  
Extracellular Vesicles ◽  
Cancer Progression ◽  
Novel Treatments ◽  
Biological Phenomena ◽  
Non Coding Rna ◽  
Non Coding Rnas ◽  
Long Non Coding Rna

Extracellular vesicles (EVs) are lipid membranous vesicles that are released from every type of cell. It has become clear that EVs are involved in a variety of biological phenomena, including cancer progression, and play critical roles in intracellular communication through the horizontal transfer of cellular cargoes such as proteins, DNA fragments, RNAs including mRNA and non-coding RNAs (microRNA, piRNA, and long non-coding RNA) and lipids. The most common cause of death associated with cancer is metastasis. Recent investigations have revealed that EVs are deeply associated with metastasis. Bone is a preferred site of metastasis, and bone metastasis is generally incurable and dramatically affects patient quality of life. Bone metastasis can cause devastating complications, including hypercalcemia, pathological fractures, spinal compression, and bone pain, which result in a poor prognosis. Although the mechanisms underlying bone metastasis have yet to be fully elucidated, increasing evidence suggests that EVs in the bone microenvironment significantly contribute to cancer progression and cancer bone tropism. Emerging evidence on EV functions in bone metastasis will facilitate the discovery of novel treatments. In this review, we will discuss the remarkable effects of EVs, especially on the tumor microenvironment in bone.

Sign in / Sign up

Export Citation Format

Share Document