Circular RNA circSLC25A16 contributes to the glycolysis of non-small-cell lung cancer through epigenetic modification

Shangguan, Hong; Hong, Feng; Lv, Dongxiao; Wang, Junfei; Tian, Tian; Wang, Xingwen

doi:10.1038/s41419-020-2635-5

Cited by 58 publications

(54 citation statements)

References 22 publications

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“…Certain circRNAs have been demonstrated to exert roles in human cancers, serving as cancer-promoting or cancer-suppressing factors [ 5 , 6 ]. Many circRNAs were reported to affect NSCLC progression, like circSLC25A16, hsa_circ_0043265, circRNA_001010 and hsa_circ_0072309 [ 7 – 10 ]. Back-spliced from aldehyde dehydrogenase 4 family member A1 (ALDH4A1), circRNA hsa_circ_0010235 (Position: chr1:19201875–19216599) was detected to be upregulated in NSCLC tissues [ 11 ], while its explicit role in NSCLC development remains to be studied.…”

Section: Introductionmentioning

confidence: 99%

Hsa_circ_0010235 functions as an oncogenic drive in non-small cell lung cancer by modulating miR-433-3p/TIPRL axis

Zhang

Cheng

et al. 2021

Cancer Cell Int

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Background Non-small cell lung cancer (NSCLC) is a threat to human health. Circular RNAs (circRNAs) have been proved to function in NSCLC development. In this study, the role of circRNA hsa_circ_0010235 in NSCLC progression and the possible molecular mechanism were explored. Methods Expression of hsa_circ_0010235, miRNA (miR)-433-3p and TOR signaling pathway regulator-like (TIPRL) was examined by quantitative real-time PCR (qRT-PCR). Cell viability and clonogenicity were detected by cell counting kit-8 (CCK-8) assay and colony formation assay, respectively. Flow cytometry was performed to monitor cell apoptosis and cell cycle distribution. Western blot assay was employed to evaluate the protein levels of TIPRL, light chain 3 (LC3)-II/I and p62. Cell metastasis was assessed by Transwell and wound healing assays. The targeted relationship between miR-433-3p and hsa_circ_0010235 or TIPRL was confirmed by dual-luciferase reporter and RNA immunoprecipitation (RIP) assays. Furthermore, the role of hsa_circ_0010235 in vivo was investigated by xenograft assay. Results Hsa_circ_0010235 and TIPRL were highly expressed in NSCLC tissues and cells, while miR-433-3p was downregulated. Depletion of hsa_circ_0010235 or gain of miR-433-3p repressed proliferation and autophagy but promoted apoptosis in NSCLC cells. Hsa_circ_0010235 sponged miR-433-3p to upregulate TIPRL expression, so as to affect NSCLC development. Hsa_circ_0010235 knockdown also blocked tumor growth in vivo. Conclusion Hsa_circ_0010235 knockdown suppressed NSCLC progression by regulating miR-433-3p/TIPRL axis, affording a novel mechanism of NSCLC progression.

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Section: Introductionmentioning

confidence: 99%

Hsa_circ_0010235 functions as an oncogenic drive in non-small cell lung cancer by modulating miR-433-3p/TIPRL axis

Zhang

Cheng

et al. 2021

Cancer Cell Int

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“…Meanwhile, circTLK1 positively regulated the expression of CBX4 by sponging miR-136-5p [29]. Additionally, circSLC25A16 functioned as a miR-488-3p sponge to suppress HIF-1α [30]. In this paper, we identi ed PDCD10 as a potential candidate gene of miR-1270 using online bioinformatic analysis.…”

Section: Discussionmentioning

confidence: 98%

CircFNDC3B inhibits cell growth in abdominal aortic aneurysm by targeting the miR-1270/PDCD10 axis

Deng¹,

Wei²,

Zhang³

et al. 2021

Preprint

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BackgroudIn certain cancers, circRNA fibronectin type III domain containing 3B (circFNDC3B) may serve as a specific target for the treatment. However, the role and underlying regulatory mechanisms of circFNDC3B in abdominal aortic aneurysm (AAA) remain unknown.MaterialsCircFNDC3B expression in AAA and normal tissues were assessed by qRT-PCR. The biological functions of circFNDC3B were evaluated by MTT, flow cytometry and Caspase-3 activity assays. Furthermore, the molecular mechanism of circFNDC3B was demonstrated by RNA immunoprecipitation (RIP), dual-luciferase reporter assay, western blotting, qRT-PCR and rescue experiments. ResultsWe found that the expression of circFNDC3B was significantly upregulated in AAA clinical specimens. Functionally, overexpression of circFNDC3B inhibited vascular smooth muscle cell (VSMC) proliferation and induced apoptosis in vitro, yet, knockdown of circFNDC3B had the opposite effects. Mechanistically, circFNDC3B upregulated the expression of programmed cell death 10 (PDCD10) by acting as a molecular sponge for miR-1270. Notably, forced expression of PDCD10 countervailed the impact of circFNDC3B knockdown on AAA biological processes.ConclusionsOur data indicated that circFNDC3B promoted the progression of AAA by targeting the miR-1270/PDCD10 pathway, and may be a potential therapeutic target in the treatment of AAA.

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“…CircSLC25A16 interacts with miR-488-3p/HIF-1α and activates LDHA by facilitating its transcription. 22 In addition, it was reported that the downregulation of serine/arginine splicing factor 1 (SRSF1) contributed to, at least in part, the increased expression of circSETD3 in NSCLC cells with acquired resistance to gefitinib in NSCLC. 23 Research has confirmed that the present research performed a circRNA microarray analysis for the expression profile and identified a novel circRNA (circMAGI3, hsa_circ_0110498).…”

Section: Discussionmentioning

confidence: 99%

Circular RNA CircCDYL Regulates Proliferation and Apoptosis in Non-Small Cell Lung Cancer Cells by Sponging miR-185-5p and Upregulating TNRC6A

Bian¹,

Xue²,

Wang³

et al. 2021

CMAR

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A series of research reveal that circular RNA (circRNA) plays a vital role in regulating the development of tumor cells. In this research, we would explore the role and mechanism of circCDYL in non-small cell lung cancer (NSCLC). Methods: RT-PCR was performed to detect the expression of circCDYL in NSCLC tissues, plasma, and cell lines. The tumor cell proliferation ability was evaluated by clone formation assay, and cell cycle determination. Flow cytometry was used to detect apoptosis in NSCLC cell lines. Western blot and RT-PCR were used to assess the expression of proteins and genes. Luciferase assay was performed to confirm the relationship of circRNA-miRNA-mRNA.Results: The decreased level of circCDYL was observed in NSCLC patients' tissues and plasma, which was also downregulated in NSCLC cell lines. Forced expression of circCDYL inhibited cell viability, proliferation and induced apoptosis in A549 cells. Luciferase assay verified that circCDYL could bind with miR-185-5p and confirmed that TNRC6A was a downstream target of miR-185-5p. Overexpression of miR-185-5p or silencing of TNRC6A could inhibit the anti-tumor effect of circCDYL in A549 cells via regulating the ERK1/2 signal. Conclusion: Here, we revealed that circCDYL inhibited proliferation and induced apoptosis in NSCLC cell lines via regulating ERK1/2 signal, and the mechanism of this progression may target miR-185-5p/TNRC6A, which provided a theoretical basis for clinical therapy.

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Circular RNA circSLC25A16 contributes to the glycolysis of non-small-cell lung cancer through epigenetic modification

Cited by 58 publications

References 22 publications

Hsa_circ_0010235 functions as an oncogenic drive in non-small cell lung cancer by modulating miR-433-3p/TIPRL axis

Hsa_circ_0010235 functions as an oncogenic drive in non-small cell lung cancer by modulating miR-433-3p/TIPRL axis

CircFNDC3B inhibits cell growth in abdominal aortic aneurysm by targeting the miR-1270/PDCD10 axis

Circular RNA CircCDYL Regulates Proliferation and Apoptosis in Non-Small Cell Lung Cancer Cells by Sponging miR-185-5p and Upregulating TNRC6A

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