Circular RNA hsa_circ_0061825 (circ‐TFF1) contributes to breast cancer progression through targeting miR‐326/TFF1 signalling

Pan, Gaofeng; Mao, Anwei; Liu, Jiazhe; Lu, Jingfeng; Ding, Jian; Liu, Weiyan

doi:10.1111/cpr.12720

Cited by 101 publications

(69 citation statements)

References 32 publications

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“…Some circRNAs, such as circGFRA1 and circ-TFF1, can bind to cognate linear transcripts to sequester mRNA from translation and thereby trigger the decrease of protein expression [ 18 , 19 ]. Here, we found that linear NOL10 expression was significantly down-regulated in BC tumor tissues compared with that in adjacent normal tissues (Additional file 1 : Figure S2A).…”

Section: Resultsmentioning

confidence: 99%

CircNOL10 suppresses breast cancer progression by sponging miR-767-5p to regulate SOCS2/JAK/STAT signaling

Wang

et al. 2021

J Biomed Sci

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Background Circular RNAs (circRNAs) have caught increasing attentions and interests for their important involvement in cancer initiation and progression. This study aims to investigate the biological functions of circNOL10 and its potential molecular mechanisms in breast cancer (BC). Materials and methods qRT-PCR and western blot assays were performed to measure the expression of related genes. CCK-8, colony formation, flow cytomerty and transwell assays were used to assess cell proliferation, cell cycle, migration and invasion. RNA pull-down, luciferase reporter and RIP assays were applied to address the potential regulatory mechanism of circNOL10. Results CircNOL10 was down-regulated in BC tissues and cells. Low expression of circNOL10 was associated with larger tumor size, advanced TNM stage, lymph node metastasis and unfavorable prognosis. Overexpression of circNOL10 inhibited cell proliferation, migration, invasion and EMT in vitro and slowed xenograft tumor growth in vivo. Mechanistically, circNOL10 could act as a molecular sponge for miR-767-5p, leading to the up-regulation of suppressors of cytokine signaling 2 (SOCS2) and inactivation of JAK2/STAT5 pathway. Moreover, circNOL10-mediated suppression of malignant phenotypes was attenuated by miR-767-5p. Similar to circNOL10, enforced expression of SOCS2 also resulted in the suppression of cell proliferation and metastasis. Furthermore, knockdown of SOCS2 reversed the tumor-suppressive effect induced by circNOL10. Conclusions CircNOL10 repressed BC development via inactivation of JAK2/STAT5 signaling by regulating miR-767-5p/SOCS2 axis. Our findings offer the possibility of exploiting circNOL10 as a therapeutic and prognostic target for BC patients.

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Section: Resultsmentioning

confidence: 99%

CircNOL10 suppresses breast cancer progression by sponging miR-767-5p to regulate SOCS2/JAK/STAT signaling

Wang

et al. 2021

J Biomed Sci

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“…Additionally, Wang et al showed that hsa_circ_0000467 could sponge miR‐326‐3p and promote gastric cancer development via enhancing cyclin D1 31 . In another study, miR‐326 interacted with circ‐TFF1 in breast cancer progression through regulating TFF1 expression 32 . These studies indicate that expression of miR‐326 is modulated by multiple circRNAs and miR‐326 holds different roles in different cancers.…”

Section: Resultsmentioning

confidence: 97%

CircRNA circ_POLA2 promotes lung cancer cell stemness via regulating the miR‐326/GNB1 axis

Fan

Bai

Zhang

et al. 2020

Environmental Toxicology

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Circular RNAs (CircRNAs) are a group of noncoding RNAs that have essential function in the development and progression of various cancers. The expression pattern and function of circRNA in lung cancer is not fully understood. In the present study, we aimed to investigate the expression profiles and underlying mechanism of circRNA circ_POLA2 in lung cancer cell stemness. Circ_POLA2 was highly expressed in lung cancer tissues and predicted a poor prognosis in lung cancer patients. Knockdown of circ_POLA2 inhibited the stemness of lung cancer cells, which is evident by the decreased sphere‐formation ability, ALDH1 activity, and stemness marker expression, but had no effects on cell viability. Mechanistically, circ_POLA2 functioned as a ceRNA by sponging miR‐326. Furthermore, miR‐326 negatively regulated G protein subunit beta 1 (GNB1) expression by targeting its 3′‐UTR (untranslated region). Intriguingly, we found that GNB1 was overexpressed and associated with poor prognosis in lung cancer patients. Overexpression of GNB1 could antagonize the inhibitory effect of circ_POLA2 knockdown on lung cancer cell stemness. In conclusion, circ_POLA2 promotes lung cancer cell stemness and progression via regulating the miR‐326/GNB1 axis, which might serve as a novel therapeutic target for lung cancer patients.

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“…Breast cancer has been a major public health problem worldwide among women ( 1 – 3 ), and thus breast cancer research has an important social significance. Recently, many related studies have shown that circ_RNF111 and circ_ABCB10 contribute to paclitaxel resistance in breast cancer ( 40 , 41 ), circ_ZEB1 acts as an oncogene in triple-negative breast cancer ( 42 ), circ_TFF1 contributes to breast cancer progression ( 43 ), circ_0000526 blocks the progression of breast cancer ( 44 ), circulating circ_RNA hsa_circ_0001785 acts as a diagnostic biomarker for breast cancer ( 45 ), etc. In the present study, the major focus was on BLBC molecular subtype, and protooncogene circ_NOTCH3 was first identified to act as a sponge for miR-205-5p, which played a crucial role in its development and progression.…”

Section: Discussionmentioning

confidence: 99%

circ_NOTCH3 Functions as a Protooncogene Competing With miR-205-5p, Modulating KLF12 Expression and Promoting the Development and Progression of Basal-Like Breast Carcinoma

Guan¹,

Zhang³

et al. 2021

Front. Oncol.

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Breast cancer is the most common type of cancer diagnosed among women, and basal-like breast carcinoma (BLBC) has been associated with a more aggressive histology, poorer prognosis, and non-responsiveness to hormone therapy. In the present study, the role and molecular mechanism of circular (circ)_NOTCH3 in the development and progression for BLBC was identified. circ_RNAs array was used to screen the ectopic expression of hsa_circ_0109177 (circ_NOTCH3) in BLBC. RT-qPCR was conducted to evaluate the circ_NOTCH3 expression in BLBC tissues and paired normal tissues, as well as related cell lines. Cell function changes were analyzed following circ_NOTCH3 or micro (mi)RNA overexpression or co-expression. Bioinformatics analysis and dual-luciferase reporter assay were performed to predict and verify the binding sites between circ_NOTCH3 and miRNAs. Gene expression changes were assessed using western blotting. circ_NOTCH3 had a significantly higher expression in BLBC tissues and cell lines. The upregulation of circ_NOTCH3 promoted the proliferation, migration, invasion and inhibited the apoptosis for BLBC cells. The opposite results were observed following miR-205-5p overexpression. However, the co-expression of circ_NOTCH3 and miR-205-5p resulted in those restoration. circ_NOTCH3 is capable of binding to miR-205-5p, and upregulating its target gene KLF12, which can be downregulated by miR-205-5p overexpression and restored by the co-expression of circ_NOTCH3 and miR205-5p. circ_NOTCH3, being an protooncogene and a powerful biomarker, can function as a sponge, compete with miR-205-5p, modulate KLF12 expression, and promote the development and progression of BLBC.

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Circular RNA hsa_circ_0061825 (circ‐TFF1) contributes to breast cancer progression through targeting miR‐326/TFF1 signalling

Cited by 101 publications

References 32 publications

CircNOL10 suppresses breast cancer progression by sponging miR-767-5p to regulate SOCS2/JAK/STAT signaling

CircNOL10 suppresses breast cancer progression by sponging miR-767-5p to regulate SOCS2/JAK/STAT signaling

CircRNA circ_POLA2 promotes lung cancer cell stemness via regulating the miR‐326/GNB1 axis

circ_NOTCH3 Functions as a Protooncogene Competing With miR-205-5p, Modulating KLF12 Expression and Promoting the Development and Progression of Basal-Like Breast Carcinoma

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