The circACC1/miR-29c-3p/FOXP1 network plays a key role in gastric cancer by regulating cell proliferation

Chen, Xiaoyuan; Liu, Chao; Ji, Le; Wang, Ning; Liu, Yanan; Wang, Min; Ruan, Litao

doi:10.1016/j.bbrc.2021.04.028

Cited by 9 publications

(4 citation statements)

References 20 publications

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“…The results of all these studies indicated that the content of functional hsa-miR-21-5p and hsa-miR-29c-3p in cells and EVs was reduced, which manifested itself in the 2-3-fold slowed proliferation of the CRISPR/Cas9-modified cells, as well as in a decrease in the antifibrotic activity of their EVs, more prominent for miR-29c-3p-edited cells. Several studies have demonstrated that miR-21 or miR-29c inhibition affects cell proliferation-for example, through the regulation of target proteins from the Ran GTPase family [13,[45][46][47][48][49][50]. This coincides with our data describing the decline in the proliferation rate of MSCs with edited hsa-mir-21 and hsa-mir-29c genes.…”

Section: Discussionsupporting

confidence: 90%

Advances and Obstacles in Using CRISPR/Cas9 Technology for Non-Coding RNA Gene Knockout in Human Mesenchymal Stromal Cells

Basalova,

Illarionova,

Skryabina

et al. 2023

ncRNA

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Non-coding RNA (ncRNAs) genes have attracted increasing attention in recent years due to their widespread involvement in physiological and pathological processes and regulatory networks. The study of the function and molecular partners of ncRNAs opens up opportunities for the early diagnosis and treatment of previously incurable diseases. However, the classical “loss-of-function” approach in ncRNA function analysis is challenged due to some specific issues. Here, we have studied the potency of two CRISPR/Cas9 variants, wild-type (SpCas9wt) and nickase (SpCas9D10A) programmable nucleases, for the editing of extended DNA sequences in human mesenchymal stromal cells (MSCs). Editing the genes of fibrosis-related hsa-miR-21-5p and hsa-miR-29c-3p, we have shown that a pair of SpCas9D10A molecules can effectively disrupt miRNA genes within the genomes of MSCs. This leads not only to a decrease in the level of knockout miRNA in MSCs and MSC-produced extracellular vesicles, but also to a change in cell physiology and the antifibrotic properties of the cell secretome. These changes correlate well with previously published data for the knockdown of certain miRNAs. The proposed approach can be used to knock out ncRNA genes within the genomes of MSCs or similar cell types in order to study their function in biological processes.

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Section: Discussionsupporting

confidence: 90%

Advances and Obstacles in Using CRISPR/Cas9 Technology for Non-Coding RNA Gene Knockout in Human Mesenchymal Stromal Cells

Basalova,

Illarionova,

Skryabina

et al. 2023

ncRNA

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“…Interestingly, multiple previous studies have demonstrated that miRNA-29c was remarkably down-regulated in gastric cancer compared with normal tissues ( Vidal et al, 2016 ; Han et al, 2015 ; Jiang et al, 2019 ; Matsuo et al, 2013 ) and the overexpression of miRNA-29c inhibits cell proliferation ( Yu et al, 2017 ) and migration ( Wang et al, 2019 ). Furthermore, multiple studies also have demonstrated that the low expression of miRNA-29c indicates poor prognosis in gastric cancer ( Chen et al, 2021 ; Y.; Han et al, 2019a ). According to the above research and considering that five of the seven target prediction programs presented miRNA-29c and LOX-binding sites, we believe that miRNA-9c is the most appropriate upstream regulatory miRNA for LOX in gastric carcinoma.…”

Section: Discussionmentioning

confidence: 99%

lncRNA/miR-29c-Mediated High Expression of LOX Can Influence the Immune Status and Chemosensitivity and Can Forecast the Poor Prognosis of Gastric Cancer

Nai

Zeng

et al. 2022

Front. Cell Dev. Biol.

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Gastric carcinoma is the fourth most prevalent cause of cancer-related deaths worldwide because of dismal prognosis and few therapeutic options. Accumulated studies have indicated that targeting lysyl oxidase (LOX) family members may serve as an anticancer strategy. Nevertheless, the specific mechanisms of LOX in stomach carcinoma are still unclear. In this study, we demonstrated that LOX is significantly different in 13 types of cancers and may act as a potential therapeutic target, especially in stomach carcinoma. Moreover, overexpression of LOX in gastric carcinoma was validated by multiple databases and contributed to the poor overall survival (OS), progression-free survival (PFS) and post-progression survival (PPS) of stomach adenocarcinoma (STAD) patients. Next, based on the ceRNA hypothesis, the HIF1A-AS2/RP11-366L20.2-miR-29c axis was characterized as the upstream regulatory mechanism of LOX gene overexpression in gastric cancer by combining correlation analysis, expression analysis, and survival analysis. Finally, we illustrated that LOX gene overexpression leads to dismal prognosis of gastric cancer, perhaps through promoting M2 macrophage polarization and tumor immune escape and enhancing drug resistance of tumor cells to chemotherapeutic drugs. Our research demonstrate that LOX may be potentially applied as a novel prognostic marker and targeting inhibition of LOX holds promise as a treatment strategy for gastric cancer.

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“…Many target mRNAs of miR-29c, including FOXP1, CDK6, NASP and CTNND1 in GC, have been discovered 9 , 25 - 27 . The modulation of miR-29c in our study revealed a crucial role in the regulation of VEGFA levels, suggesting that it is a molecular regulator of metastatic function via miR-29c/VEGFA signaling.…”

Section: Discussionmentioning

confidence: 99%

miR-29c inhibits metastasis of gastric cancer cells by targeting VEGFA

Yu¹,

Zhu²,

Fan³

et al. 2022

J. Cancer

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Background: Gastric cancer (GC) is characterized by tissue invasion and metastasis, which lead to an aggressive and highly lethal disease. However, the underlying molecular mechanism remains largely unclear. Although multiple miRNAs are known to regulate crucial cellular events during cancer metastasis, their individual roles are still not fully described. Methods: miR-29c overexpressed cell lines were constructed. The wound healing, migration and invasion assays were performed to investigate the effect of miR-29c on metastasis of GC. HUVECs proliferation and tube formation assays were used to test the ability of angiogenesis of miR-29c. The target gene VEGFA was predicted by bioinformatic algorithms and validated by luciferase activity assay. Peritoneal spreading and pulmonary metastasis mice models were applied in vivo. Results: In the current study, we report the results that introduction of exogenous miR-29c inhibits GC cell migration, invasion and angiogenesis. Epithelial-mesenchymal transition (EMT) and cancer stem cells (CSCs) properties are participated in the miR-29c mediated cell metastasis. Furthermore, by performing tumor metastasis PCR array and luciferase reporter assay, we find that the expression of VEGFA is regulated by miR-29c through direct targeting of its 3'-UTR. In addition, we show that the VEGFA/VEGFR2/ERK pathway is involved in this process. Conclusion: These data taken together reveal the crucial functions of miR-29c-VEGFA/VEGFR2/ERK signaling axis in the metastasis progression of GC via regulating EMT and CSCs properties, which make them potential targets for clinical intervention in GC.

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The circACC1/miR-29c-3p/FOXP1 network plays a key role in gastric cancer by regulating cell proliferation

Cited by 9 publications

References 20 publications

Advances and Obstacles in Using CRISPR/Cas9 Technology for Non-Coding RNA Gene Knockout in Human Mesenchymal Stromal Cells

Advances and Obstacles in Using CRISPR/Cas9 Technology for Non-Coding RNA Gene Knockout in Human Mesenchymal Stromal Cells

lncRNA/miR-29c-Mediated High Expression of LOX Can Influence the Immune Status and Chemosensitivity and Can Forecast the Poor Prognosis of Gastric Cancer

miR-29c inhibits metastasis of gastric cancer cells by targeting VEGFA

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