Hsa_hsa_circ_0081069 promotes the progression of colorectal cancer through sponging <scp>miR</scp>‐665 and regulating <scp>E2F3</scp> expression

Xie, Jingjing; Jin, Dan; Xu, Jinyin; Yang, Fei; Jin, Jianying

doi:10.1002/jcla.24710

Cited by 7 publications

(3 citation statements)

References 41 publications

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“…Based on database prediction and experiment verification, we confirmed that miR-665 participated in circSIPA1L3-mediated regulation on the SLC16A1 and RAB11A expression. The functional roles of miR-665 are not consistent in different cancers, which might be attributed to diverse upstream signaling [56,57]. Our findings reported the tumor suppressive role of miR-665 in breast cancer, which is under rigorous regulation and participates in the induced malignant behaviors of circSIPA1L3.…”

Section: Discussionmentioning

confidence: 67%

Exosomal circSIPA1L3-mediated intercellular communication contributes to glucose metabolic reprogramming and progression of triple negative breast cancer

Liang,

Ye,

Luo

et al. 2024

Mol Cancer

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Background Breast cancer is the most common malignant tumor, and metastasis remains the major cause of poor prognosis. Glucose metabolic reprogramming is one of the prominent hallmarks in cancer, providing nutrients and energy to support dramatically elevated tumor growth and metastasis. Nevertheless, the potential mechanistic links between glycolysis and breast cancer progression have not been thoroughly elucidated. Methods RNA-seq analysis was used to identify glucose metabolism-related circRNAs. The expression of circSIPA1L3 in breast cancer tissues and serum was examined by qRT-PCR, and further assessed its diagnostic value. We also evaluated the prognostic potential of circSIPA1L3 by analyzing a cohort of 238 breast cancer patients. Gain- and loss-of-function experiments, transcriptomic analysis, and molecular biology experiments were conducted to explore the biological function and regulatory mechanism of circSIPA1L3. Results Using RNA-seq analysis, circSIPA1L3 was identified as the critical mediator responsible for metabolic adaption upon energy stress. Gain- and loss-of-function experiments revealed that circSIPA1L3 exerted a stimulative effect on breast cancer progression and glycolysis, which could also be transported by exosomes and facilitated malignant behaviors among breast cancer cells. Significantly, the elevated lactate secretion caused by circSIPA1L3-mediated glycolysis enhancement promoted the recruitment of tumor associated macrophage and their tumor-promoting roles. Mechanistically, EIF4A3 induced the cyclization and cytoplasmic export of circSIPA1L3, which inhibited ubiquitin-mediated IGF2BP3 degradation through enhancing the UPS7-IGF2BP3 interaction. Furthermore, circSIPA1L3 increased mRNA stability of the lactate export carrier SLC16A1 and the glucose intake enhancer RAB11A through either strengthening their interaction with IGF2BP3 or sponging miR-665, leading to enhanced glycolytic metabolism. Clinically, elevated circSIPA1L3 expression indicated unfavorable prognosis base on the cohort of 238 breast cancer patients. Moreover, circSIPA1L3 was highly expressed in the serum of breast cancer patients and exhibited high diagnostic value for breast cancer patients. Conclusions Our study highlights the oncogenic role of circSIPA1L3 through mediating glucose metabolism, which might serve as a promising diagnostic and prognostic biomarker and potential therapeutic target for breast cancer.

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Section: Discussionmentioning

confidence: 67%

Exosomal circSIPA1L3-mediated intercellular communication contributes to glucose metabolic reprogramming and progression of triple negative breast cancer

Liang,

Ye,

Luo

et al. 2024

Mol Cancer

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“…CircSDHC and circPRKC1 both have been shown to facilitates the proliferation and metastasis of renal cell carcinoma and lung adenocarcinoma by sponging miR‐127‐3p, miR‐545 and miR‐589 functions, respectively 14 . Likewise, hsa_circ_0043278 and hsa_circ_0003645 were shown to be associated with advanced clinical progression and metastasis of NSCLC by sponging miR‐520f and miR‐1179 15 …”

Section: Introductionmentioning

confidence: 99%

“…14 Likewise, hsa_circ_0043278 and hsa_circ_0003645 were shown to be associated with advanced clinical progression and metastasis of NSCLC by sponging miR-520f and miR-1179. 15 Recently, few studies have reported that upregulated hsa_ circ0088036 promoted rheumatoid arthritis (RA) progression, indicating its potential for application as diagnostic and therapeutic biomarker. 16,17 However, clinical expression levels and detailed molecular mechanisms of hsa_circ0088036 underlying NSCLC development had not been investigated.…”

Section: Introductionmentioning

confidence: 99%

Hsa_circ_0088036 promotes nonsmall cell lung cancer progression by regulating miR‐1343‐3p/Bcl‐3 axis through TGFβ/Smad3/EMT signaling

Chen

Liu

et al. 2023

Molecular Carcinogenesis

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Nonsmall cell lung cancer (NSCLC) is the leading cause of cancer‐related mortality worldwide. Circular RNAs (circRNAs) have been the focus of numerous studies, and some circRNAs have been linked to the development of multiple malignant tumors, including NSCLC. Nevertheless, the functional role and mechanisms of circRNAs in NSCLC remain largely unknown. The primary objective of this study was to screen the associated circRNA in NSCLC and investigate its mechanism. CircRNA microarray was used to identify circRNAs that were abnormally expressed in NSCLC tissue samples. Expression of hsa_circRNA_0088036 was validated in NSCLC tissues and cell lines after the correlation between hsa_circRNA_0088036 and prognosis was determined. We then used a series of function gain‐and‐loss assays to determine the role of hsa_circ_0088036 in NSCLC progression. RNA‐binding protein immunoprecipitation (RIP), RNA pull‐down, and RNA interference assays were used to assess the interaction between hsa_circ_0088036 and miR‐1343‐3p/Bcl‐3 axis. Moreover, mechanistic assays were applied to investigate the involved signaling pathway regulated by the hsa_circ_0088036/miR‐1343‐3p/Bcl‐3 axis. Microarray analysis and reverse transcription polymerase chain reaction confirmed the presence of a circRNA termed hsa_circ 0088036 that was upregulated in NSCLC tissue samples and cell lines and indicated a positive association with patient prognosis. Functionally, hsa_circ_0088036 silencing inhibited proliferative, invasive, and migrative potential of NSCLC cells as well as epithelial‐mesenchymal transition (EMT)‐related proteins by sponging miR‐1343‐3p to inhibit Bcl‐3. Furthermore, mechanistic experiments demonstrated that hsa_circ_0088036 promoted NSCLC progression by activating the TGFβ/Smad3/EMT signaling pathway via miR‐1343‐3p/Bcl‐3 axis. In conclusion, hsa_circ_0088036 functions as an oncogene by targeting the miR‐1343‐3p/Bcl‐3 axis via TGFβ/Smad3/EMT signaling pathway.

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Exosome‐transported of circ_0081069 induces SPIN1 production by binding to miR‐195‐5p to inhibit radiosensitivity in esophageal squamous cell carcinoma

Chai,

Liu,

Liu

et al. 2024

J Biochem & Molecular Tox

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Circ_0081069 plays a key role in tumor growth; however, its effect on radiosensitivity in esophageal squamous cell carcinoma (ESCC) remains unknown. The study is performed to reveal the association of circ_0081069 expression and radiosensitivity in ESCC and the underlying mechanism. Circ_0081069, miR‐195‐5p, and spindlin 1 (SPIN1) RNA expression were detected by quantitative real‐time polymerase chain reaction. Protein expression was checked by Western blot analysis or immunohistochemistry assay. Cell viability, proliferation, cell apoptosis, migration, and invasion were investigated by cell counting kit‐8, 5‐Ethynyl‐29‐deoxyuridine, flow cytometry analysis, scratch test, and transwell assays, respectively. The sensitivity of ESCC cells to radiation was investigated by cell colony formation assay. The interactions among circ_0081069, miR‐195‐5p, and SPIN1 were identified by dual‐luciferase reporter assay and RNA Immunoprecipitation assay. Xenograft mouse model assay was performed to determine the effect of circ_0007841 on radiosensitivity in vivo. Circ_0081069 and SPIN1 expression were upregulated, whereas miR‐195‐5p was downregulated in ESCC tissues, ESCC cells, and radiation‐stimulated ESCC cells. Circ_0081069 silencing inhibited ESCC cell proliferation, invasion, and migration but improved cell apoptosis. In addition, circ_0081069 knockdown enhanced ESCC cell radiosensitivity in vitro and in vivo. Circ_0081069 bound to miR‐195‐5p and regulated radiosensitivity by binding to miR‐195‐5p in ESCC cells. Moreover, SPIN1, a target of miR‐195‐5p, rescued miR‐195‐5p‐mediated effects in ESCC cells. Circ_0081069 was secreted from ESCC cells by being packaged into exosomes. Further, circ_0081069‐Exo inhibited radiosensitivity in ESCC cells. Exosome‐mediated transfer of circ_0081069 induced SPIN1 production by binding to miR‐195‐5p, further inhibiting radiosensitivity in ESCC.

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Hsa_hsa_circ_0081069 promotes the progression of colorectal cancer through sponging miR‐665 and regulating E2F3 expression

Cited by 7 publications

References 41 publications

Exosomal circSIPA1L3-mediated intercellular communication contributes to glucose metabolic reprogramming and progression of triple negative breast cancer

Exosomal circSIPA1L3-mediated intercellular communication contributes to glucose metabolic reprogramming and progression of triple negative breast cancer

Hsa_circ_0088036 promotes nonsmall cell lung cancer progression by regulating miR‐1343‐3p/Bcl‐3 axis through TGFβ/Smad3/EMT signaling

Exosome‐transported of circ_0081069 induces SPIN1 production by binding to miR‐195‐5p to inhibit radiosensitivity in esophageal squamous cell carcinoma

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