High circ-SEC31A expression predicts unfavorable prognoses in non-small cell lung cancer by regulating the miR-520a-5p/GOT-2 axis

Jin, Mingming; Shi, Chunzi; Hua, Qian; Tian, Li; Yang, Chen; Wu, Yue; Zhao, Leilei; Yang, Hao; Zhang, Jiaqi; Hu, Cheng; Huang, Gang

doi:10.18632/aging.103264

Cited by 15 publications

(15 citation statements)

References 60 publications

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“…Here, we demonstrated the remarkable overexpression of circSEC31A in NSCLC, consistent with previous work. 12 As has been reported for other circRNAs, 16,17 circSEC31A was unusually stable and resistant to RNase R, owing to the lack of both 5ʹ and 3ʹ ends. 18 As a hallmark of cancer biology, the enhanced glycolysis can satisfy the increasing energy requirement of cancer cells and promote cancer development.…”

Section: Discussionmentioning

confidence: 55%

“… 10 , 11 More importantly, circRNA SEC31A (circSEC31A, hsa_circ_0001421), derived from the backsplice of SEC31A gene, was found to be overexpressed in NSCLC tumor tissues and contribute to NSCLC progression. 12 Although this report also uncovered a regulatory mechanism of circSEC31A in NSCLC, our understanding of its molecular basis is still limited. Intriguingly, when we utilized computer algorithms to identify the molecular basis underlying the involvement of circSEC31A in NSCLC, we found a potential regulatory network, the circSEC31A/miR-376a/SEC31A axis.…”

Section: Introductionmentioning

confidence: 89%

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<p>CircSEC31A Promotes the Malignant Progression of Non-Small Cell Lung Cancer Through Regulating SEC31A Expression via Sponging miR-376a</p>

Cheng¹,

Yu²,

Zhang³

et al. 2020

CMAR

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Background Circular RNAs (circRNAs) have recently been shown as important regulators in the pathogenesis of non-small cell lung cancer (NSCLC). The purpose of this work was to explore the precise parts played by circRNA SEC31 homolog A (circSEC31A, hsa_circ_0001421) in NSCLC malignant progression. Methods The expression levels of circSEC31A, miR-376a and SEC31 homolog A (SEC31A) were gauged by quantitative real-time polymerase chain reaction (qRT-PCR) or Western blot. Subcellular fractionation assay was used to determine the subcellular localization of circSEC31A, and RNase R assay was performed to assess the stability of circSEC31A. Cell migration and invasion were detected by transwell assay, and cell apoptosis was evaluated using flow cytometry. Measurement of glucose consumption, lactate production and adenosine triphosphate (ATP) level were done using corresponding assay kits. The targeted interactions among circSEC31A, miR-376a and SEC31A were confirmed by the dual-luciferase reporter and RNA pull-down assays. Animal studies were performed to observe the role of circSEC31A in tumor growth in vivo. Results Our data indicated that circSEC31A and SEC31A were upregulated in NSCLC tissues and cells. CircSEC31A knockdown suppressed NSCLC cell migration, invasion, glycolysis and promoted apoptosis in vitro, as well as hindered tumor growth in vivo. Mechanistically, circSEC31A directly interacted with miR-376a, and circSEC31A depletion regulated NSCLC cell malignant progression by miR-376a. Moreover, SEC31A was a functional target of miR-376a, and it mediated the regulatory impact of miR-376a overexpression on NSCLC cell progression. Furthermore, circSEC31A controlled SEC31A expression through acting as a miR-376a sponge. Conclusion Our findings first identified that the knockdown of circSEC31A suppressed NSCLC malignant progression at least partly through modulating SEC31A expression by acting as a miR-376a sponge, providing a novel molecular target of NSCLC therapy.

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Section: Discussionmentioning

confidence: 55%

Section: Introductionmentioning

confidence: 89%

<p>CircSEC31A Promotes the Malignant Progression of Non-Small Cell Lung Cancer Through Regulating SEC31A Expression via Sponging miR-376a</p>

Cheng¹,

Yu²,

Zhang³

et al. 2020

CMAR

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“…The results in the present study further corroborate the tumor-inhibiting effect of miR-520a-5p in NSCLC cells. CDK4 ( 53 ), GOT-2 ( 54 ), ORMDL3 ( 52 ) and STAT3 are proven targets of miR-520a-5p. Therefore, the putative target of miR-520a-5p was investigated and HMGA1 was selected for experimental confirmation as a result of its crucial regulatory effects on NSCLC progression ( 31 - 34 ).…”

Section: Discussionmentioning

confidence: 99%

Long non‑coding RNA LINC01748 exerts carcinogenic effects in non‑small cell lung cancer cell lines by regulating the microRNA‑520a‑5p/HMGA1 axis

Tan

et al. 2021

Int J Mol Med

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The important functions of long non-coding RNAs in the malignancy of non-small cell lung cancer (NSCLC) has been increasingly highlighted. However, whether LINC01748 functions in a crucial regulatory role still requires further research. The aim of the present study was to investigate the biological roles of LINC01748 in NSCLC. Furthermore, different experiments were utilized to investigate the mechanism of action of LINC01748 in 2 NSCLC cell lines. Reverse transcription-quantitative PCR was used to measure mRNA expression levels. Cell Counting Kit-8 assay, flow cytometry analysis and Transwell and Matrigel assays were also used to analyze, cell viability, apoptosis, and migration and invasion, respectively. A tumor xenograft model was used for in vivo experiments. RNA immunoprecipitation experiments, luciferase reporter assays and rescue experiments were used to investigate the mechanisms involved. Data from The Cancer Genome Atlas dataset and patients recruited into the present study showed that LINC01748 was overexpressed in NSCLC. Patients with high LINC01748 mRNA expression level had shorter overall survival rate compared with that in patients with low LINC01748 mRNA expression level. Then, knockdown of LINC01748 mRNA expression level reduced cell proliferation, migration and invasion, but increased cell apoptosis in vitro . Knockdown of LINC01748 also reduced tumor growth in vivo . Mechanistically, LINC01748 could act as a competing endogenous (ce)RNA to sponge microRNA(miR)-520a-5p, to increase the expression level of the target gene, high mobility group AT-hook 1 (HMGA1) in the NSCLC cell lines. Furthermore, rescue experiments illustrated that the functions exerted by LINC01748 knockdown were negated by miR-520a-5p inhibition or HMGA1 overexpression. In summary, LINC01748 acted as a ceRNA by sponging miR-520a-5p, leading to HMGA1 overexpression, thus increasing the aggressiveness of the NSCLC cells. Accordingly, targeting the LINC01748/miR-520a-5p/HMGA1 pathway may benefit NSCLC therapy.

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“…12 For instance, circ-SEC31A is the ceRNA for miR-520a-5p to promote lung cancer progression. 19 Hsa_circ_103809 plays an oncogenic function in gastric cancer through interacting with miR-101-3p. 20 In addition, circ-CSPP1 contributes to HCC growth and invasion through sponging miR-577.…”

Section: Discussionmentioning

confidence: 99%

Circ_0072995 Promotes Proliferation and Invasion via Regulating miR-1253/EIF4A3 Signaling in HCC

He¹,

Tao²,

Xu³

et al. 2021

CMAR

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Background: Hepatocellular carcinoma (HCC) is a major threat for human health. This work aimed to determine the potential function of circ_0072995 in HCC progression and its molecular mechanism. Methods: qRT-PCR was conducted to analyze circ_0072995 expression. CCK8 and colony formation assays were utilized to detect cell proliferation. Transwell assay was performed to determine migration and invasion. Interactions among circ_0072995, miR-1253 and EIF4A3 (Eukaryotic Translation Initiation Factor 4A3) were predicted through bioinformatics methods and confirmed via luciferase reporter assay and RNA pulldown assay. Results: circ_0072995 expression was upregulated in HCC tissues. Circ_0072995 high level was associated with poor prognosis. Circ_0072995 knockdown impaired proliferation, migration, invasion and survival. MiR-1253 was sponged by circ_0072995 and targeted EIF4A3 directly. Circ_0072995 inhibited miR-1253 to upregulate EIF4A3 level. Conclusion: Circ_0072995 exerted tumorigenic roles to enhance HCC progression through activating EIF4A3 by sponging miR-1253.

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High circ-SEC31A expression predicts unfavorable prognoses in non-small cell lung cancer by regulating the miR-520a-5p/GOT-2 axis

Cited by 15 publications

References 60 publications

<p>CircSEC31A Promotes the Malignant Progression of Non-Small Cell Lung Cancer Through Regulating SEC31A Expression via Sponging miR-376a</p>

<p>CircSEC31A Promotes the Malignant Progression of Non-Small Cell Lung Cancer Through Regulating SEC31A Expression via Sponging miR-376a</p>

Long non‑coding RNA LINC01748 exerts carcinogenic effects in non‑small cell lung cancer cell lines by regulating the microRNA‑520a‑5p/HMGA1 axis

Circ_0072995 Promotes Proliferation and Invasion via Regulating miR-1253/EIF4A3 Signaling in HCC

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