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Review
. 2015 Feb;36(2):521-32.
doi: 10.1007/s13277-015-3136-5. Epub 2015 Feb 1.

The functional sites of miRNAs and lncRNAs in gastric carcinogenesis

Affiliations
Review

The functional sites of miRNAs and lncRNAs in gastric carcinogenesis

Xiangxiang Wan et al. Tumour Biol. 2015 Feb.

Abstract

Gastric cancer is one of the most common malignant diseases and has one of the highest mortality rates worldwide. Its molecular mechanisms are poorly understood. Recently, the functions of non-coding RNAs (ncRNAs) in gastric cancer have attracted wide attention. Although the expression levels of various ncRNAs are different, they may work together in a network and contribute to gastric carcinogenesis by altering the expression of oncogenes or tumor suppressor genes. They affect the cell cycle, apoptosis, motility, invasion, and metastasis. Dysregulated microRNAs (miRNAs) and long non-coding RNAs (lncRNAs), including miR-21, miR-106, H19, and ANRIL, directly or indirectly regulate carcinogenic factors or signaling pathways such as PTEN, CDK, caspase, E-cadherin, Akt, and P53. Greater recognition of the roles of miRNAs and lncRNAs in gastric carcinogenesis can provide new insight into the mechanisms of tumor development and identify targets for anticancer drug development.

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Figures

Fig 1
Fig 1
ncRNAs affect Akt pathway in cell cycle. MiRNAs and lncRNAs affect gastric cancer cell cycle progression. By regulating Akt pathway, onco-ncRNAs promote gastric cancer cell growth. Conversely, tumor suppressor ncRNAs suppress the gastric cancer cell cycle
Fig 2
Fig 2
ncRNAs affect CDKIs and Myc pathway in cell cycle. MiRNAs and lncRNAs affect gastric cancer cell cycle progression. By regulating CDKIs and their downstream and Myc pathway, onco-ncRNAs promote gastric cancer cell growth. Conversely, tumor suppressor ncRNAs suppress the gastric cancer cell cycle
Fig 3
Fig 3
ncRNAs associated with apoptosis in GC. MiRNAs and lncRNAs affect gastric cancer cell apoptosis. By regulating extrinsic and intrinsic pathways, onco-ncRNAs suppress gastric cancer apoptosis. Conversely, tumor suppressor ncRNAs promote gastric cancer cell apoptosis
Fig 4
Fig 4
ncRNAs associated with EMT in GC. MiRNAs and lncRNAs affect gastric cancer cell metastasis. By regulating EMT, onco-ncRNAs promote gastric cancer cell metastasis. Conversely, tumor suppressor ncRNAs suppress gastric cancer cell metastasis
Fig 5
Fig 5
Degradation of ECM by ncRNAs in GC. MiRNAs and lncRNAs affect gastric cancer cell metastasis. By regulating remodeling of ECM, onco-ncRNAs promote gastric cancer cell metastasis. Conversely, tumor suppressor ncRNAs suppress gastric cancer cell metastasis
Fig 6
Fig 6
Angiogenesis by ncRNAs in GC. MiRNAs and lncRNAs affect gastric cancer cell metastasis. By regulating angiogenesis, onco-ncRNAs promote gastric cancer cell metastasis. Conversely, tumor suppressor ncRNAs suppress gastric cancer cell metastasis

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