Long Noncoding RNA (lncRNA)-Mediated Competing Endogenous RNA Networks Provide Novel Potential Biomarkers and Therapeutic Targets for Colorectal Cancer

Wang, Liye; Cho, Kwang Bog; Li, Yan; Tao, Gabriel; Xie, Zuoxu; Guo, Bin

doi:10.3390/ijms20225758

Cited by 429 publications

(331 citation statements)

References 187 publications

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“…Increasing numbers of studies have identified that lncRNA, microRNA (miRNA), and protein-coding message RNA (mRNA) compose complex RNA networks by competitive association. Abnormal regulation or aberrant expression of various lncRNA plays a role in the initiation, progression, and relapse of colorectal cancer (2,3).…”

Section: Introductionmentioning

confidence: 99%

Long Non-coding RNA MIR570MG Causes Regorafenib Resistance in Colon Cancer by Repressing miR-145/SMAD3 Signaling

Fang

Wang

et al. 2020

Front. Oncol.

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An increasing number of studies have shown that long non-coding RNA (lncRNA) dysregulation plays a fundamental role in the development of various cancers, including colon cancer. Nonetheless, the mechanisms of lncRNA in regorafenib-resistance remain unclear. Our research revealed the lncRNA MIR570MG increased in regorafenib-resistant colon cancer cells compared to the regorafenib-sensitive cells. Furthermore, MIR570MG sponged miR-145, which declined in regorafenib-resistant colon cancer cell lines. More importantly, overexpression of miR-145 hampered cell proliferation and retrieved colon cancer regorafenib-sensitivity, contrary to the function of MIR570MG. Dual-luciferase reporter assay confirmed that miR-145 bound to 3 ′-UTR of SMAD3, a transcriptional modulator activated by TGFβ, resulting in blockage of TGFβ /SMAD3-mediated cell growth and cycle progression. Besides, ectopic expression of miR-145 inhibitor in the parental cells endowed resistance to regorafenib. Inversely, knockdown of MIR570MG impoverished resistance against regorafenib. Additionally, overexpression of MIR570MG conquered the suppression of tumor growth by miR-146 and rehabilitated the resistance to regorafenib in HCT116R human colon cancer mouse models. In summary, our findings suggested that MIR570MG promoted regorafenib resistance via releasing SMAD3 from miR-145, leading to activation of SMAD3-mediated signaling pathways.

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Section: Introductionmentioning

confidence: 99%

Long Non-coding RNA MIR570MG Causes Regorafenib Resistance in Colon Cancer by Repressing miR-145/SMAD3 Signaling

Fang

Wang

et al. 2020

Front. Oncol.

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“…The competing endogenous RNAs (ceRNAs) hypothesis proposes a novel regulatory network involving lncRNAs, miRNAs, circular RNAs (circRNAs) and pseudogenes, and such a network is of great signi cance in tumor formation and progression [31]. Accumulating evidence demonstrated that lncRNAs exerted biological roles in various tumors by functioning as ceRNAs for sponging miRNA to modulating miRNAs' target gene expression [32].…”

Section: Discussionmentioning

confidence: 99%

LncRNA FAM83H-AS1 Promotes Aerobic Glycolysis and Tumor Progression by Regulating miR-4684-5p/ZBTB38 Axis in Esophageal Squamous Cell Carcinoma

Qian

Chen

et al. 2020

Preprint

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Background: Dysregulation of lncRNAs is implicated in esophageal squamous cell carcinoma (ESCC) progression; However, the precise function of lncRNA FAM83H-AS1 in ESCC remains unknown. Methods: FAM83H-AS1, miR-4684-5p and ZBTB38 mRNA expressions were detected via qRT-PCR. ZBTB38, GLUT1 and LDH-A protein expressions were tested via Western blot. Cell proliferation, migration and invasion were evaluated via CCK-8 and transwell assay, respectively. A nude mouse xenograft model was used to investigate the role of FAM83H-AS1 in xenograft ESCC growth. The metabolic shift in ESCC cells was examined via glycolysis analysis. The interaction between FAM83H-AS1, miR-4684-5p and ZBTB38 was analyzed via computational algorithms, RNA pull-down, RIP and dual luciferase reporter assay. Results: We found that FAM83H-AS1 was upmodulated in ESCC cell lines. FAM83H-AS1 knockdown hampered ESCC cell proliferation, migration, invasion and aerobic glycolysis, while FAM83H-AS1 overexpression demonstrated the opposite effects. FAM83H-AS1 knockdown also delayed the tumor growth in vivo. Moreover, FAM83H-AS1 interacted with miR-4684-5p/ZBTB38 axis in ESCC cells. ZBTB38 overexpression or miR-4684-5p inhibition partially reversed the inhibitory effect of FAM83H-AS1 knockdown on cell migration, invasion and aerobic glycolysis in ESCC cells. Conclusion: Our present results indicate FAM83H-AS1 accelerated aerobic glycolysis and tumorigenesis of ESCC by sponging miR-4684-5p and triggering the expression of ZBTB38, providing new insights into mechanism of ESCC progression and therapeutic strategy.

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“…It has been shown previously that lncRNAs may function as ceRNAs to interact with miRNAs in the cytoplasm, thereby reducing the suppressive action of miRNAs on their targets. 25 In order to investigate whether CASC19 acts as a ceRNA, we first determined the expression distribution of CASC19 in 786-O and A498 cells. Subcellular fractionation location plus RT-qPCR analysis indicated that CASC19 was mainly distributed in the cytoplasm of 786-O and A498 cells ( Figure 3A).Next, bioinformatics analysis was employed to search for the miRNAs that might potentially interact with CASC19.…”

Section: Knockdown Of Casc19 Attenuates Ccrcc Cell Proliferation Colmentioning

confidence: 99%

<p>Long Non-Coding RNA <em>CASC19</em> Sponges microRNA-532 and Promotes Oncogenicity of Clear Cell Renal Cell Carcinoma by Increasing ETS1 Expression</p>

Luo¹,

Liu²,

Yan³

et al. 2020

CMAR

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Purpose: The long non-coding RNA cancer susceptibility 19 (CASC19) is recognized as an important regulator in gastric cancer, colorectal cancer, and non-small cell lung cancer. Nevertheless, to the best of our knowledge, the expression status and detailed roles of CASC19 in clear cell renal cell carcinoma (ccRCC) have not been elucidated. Hence, we aimed to determine CASC19 expression in ccRCC and investigate its roles in ccRCC oncogenicity. The molecular mechanisms underlying CASC19 functions in ccRCC were also determined. Methods: CASC19 expression was measured by using reverse transcription-quantitative polymerase chain reaction. The effects of CASC19 on ccRCC cell proliferation, colony formation, migration, and invasiveness in vitro, as well as on tumor growth in vivo, were examined by the MTT assay, colony formation assay, cell migration and invasiveness assays, and tumor xenograft in nude nice, respectively. Results: CASC19 was overexpressed in ccRCC tissues and cell lines. High expression of CASC19 was closely associated with unfavorable clinicopathological parameters and predicted negative clinical outcomes in patients with ccRCC. Knockdown of CASC19 decreased ccRCC cell proliferation, colony formation, migration, and invasiveness, as well as attenuated tumor growth in vivo. Mechanistically, CASC19 functioned as a competing endogenous RNA and upregulated the expression of ETS proto-oncogene 1 (ETS1) through sponging microRNA-532 (miR-532). Furthermore, rescue assays revealed that inhibiting miR-532 or restoring ETS1 expression partially abolished the impacts of CASC19 knockdown on ccRCC cells. Conclusion: The CASC19/miR-532/ETS1 regulatory pathway is crucial for the malignant manifestations of ccRCC, which makes it an attractive target for potential treatments of ccRCC.

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Long Noncoding RNA (lncRNA)-Mediated Competing Endogenous RNA Networks Provide Novel Potential Biomarkers and Therapeutic Targets for Colorectal Cancer

Cited by 429 publications

References 187 publications

Long Non-coding RNA MIR570MG Causes Regorafenib Resistance in Colon Cancer by Repressing miR-145/SMAD3 Signaling

Long Non-coding RNA MIR570MG Causes Regorafenib Resistance in Colon Cancer by Repressing miR-145/SMAD3 Signaling

LncRNA FAM83H-AS1 Promotes Aerobic Glycolysis and Tumor Progression by Regulating miR-4684-5p/ZBTB38 Axis in Esophageal Squamous Cell Carcinoma

<p>Long Non-Coding RNA <em>CASC19</em> Sponges microRNA-532 and Promotes Oncogenicity of Clear Cell Renal Cell Carcinoma by Increasing ETS1 Expression</p>

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