Circ_0000735 enhances the proliferation, metastasis and glycolysis of non-small cell lung cancer by regulating the miR-635/FAM83F axis

Tai, Guigang; Zhang, Miao; Liu, Fang

doi:10.1080/01902148.2021.1881188

Cited by 11 publications

(8 citation statements)

References 27 publications

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“…Sequence Similarity Family 83 (FAM83) contains eight genes from FAM83A to FAM83H, and members of this family are promoters of multiple human tumors, such as esophageal squamous cell carcinoma and pancreatic ductal adenocarcinoma [33–35]. In this study, FAM83F was confirmed to be significantly elevated in NSCLC tissues and cells, which was consistent with previous studies [36,37]. We also observed for the first time that the level of FAM83F in PTX-resistant NSCLC cells was significantly higher than in the corresponding parental cells (A549 and H1299).…”

Section: Discussionsupporting

confidence: 91%

Blocking circ_0010235 suppresses acquired paclitaxel resistance of non-small cell lung cancer by sponging miR-512-5p to modulate FAM83F expression

Luo

et al. 2022

Anti-Cancer Drugs

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The occurrence of paclitaxel (PTX) resistance in nonsmall cell lung cancer (NSCLC) is a major challenge for NSCLC treatment. Circular RNAs (circRNAs) have been reported to associate with cancer resistance, but the role of circ_0010235 in PTX resistance of NSCLC is unclear. The expression of circ_0010235 and microRNA-512-5p (miR-512-5p) were determined by quantitative real-time PCR. Cell counting kit-8 assay, transwell assay and flow cytometry were performed to measure the PTX resistance, proliferation, migration, invasion and apoptosis of cells. All proteins were assessed via western blot analysis. The combination between miR-512-5p and circ_0010235 or FAM83F was predicted by the online database and confirmed by a dual-luciferase reporter assay. Angiogenesis assay was used to detect the ability of cells to form blood vessels. Animal experiments were employed to confirm the effect of circ_0010235 on NSCLC tumor growth in vivo. Circ_0010235 and FAM83F were upregulated in PTX-resistant NSCLC tissues and cells. Circ_0010235 knockdown suppressed the resistance to PTX, proliferation, angiogenesis and migration/invasion in A549/PTX and H1299/PTX cells but promoted apoptosis rate. MiR-512-5p could be sponged by circ_0010235, and its overexpression had an inhibition effect on the PTX resistance of NSCLC cells. FAM83F was a target of miR-512-5p and circ_0010235 could modulate FAM83F expression by sponging miR-512-5p. In vivo experiments revealed that silenced circ_0010235 could improve the sensitivity of the tumor to PTX. Therefore, these findings advocated targeting the circ_0010235/miR-512-5p/ FAM83F axis as a potential therapeutic option for patients with NSCLC who are resistant to PTX. Anti-Cancer Drugs 33: 1024

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Section: Discussionsupporting

confidence: 91%

Blocking circ_0010235 suppresses acquired paclitaxel resistance of non-small cell lung cancer by sponging miR-512-5p to modulate FAM83F expression

Luo

et al. 2022

Anti-Cancer Drugs

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“…MiR‐635 is related to the progression of NSCLC 24 . Tai et al explained that circ_0000735 promotes the progress of NSCLC through miR‐635 / FAM83F axis 25 . In this study, miR‐635 was decreased in NSCLC tissues or cells and mainly played an inhibitory role in NSCLC.…”

Section: Discussionmentioning

confidence: 99%

Circ_0102231 inactivates the PI3K/AKT signaling pathway by regulating the miR‐635/NOVA2 pathway to promote the progression of non‐small cell lung cancer

Liu,

Yu,

Yang

2023

Thoracic Cancer

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BackgroundCircular RNAs (circRNAs) are involved in the malignant development of tumors. However, the mechanism of circ_0102231 in non‐small cell lung cancer (NSCLC) has rarely been discussed and reported.MethodsQuantitative real‐time polymerase chain reaction (qRT‐PCR) was used to measure the expression of circ_0102231, miR‐635 and NOVA alternative splicing regulator 2 (NOVA2) in NSCLC tissues and cells. Western blot was applied to detect the protein expression. Cell proliferation was monitored by cell counting kit‐8 (CCK8) and 5‐ethynyl‐2′‐deoxyuridine (EdU) experiments. The angiogenesis ability of cells was tested by angiogenesis assay. Flow cytometry was used to analyze cell apoptosis. The relationship between circ_0102231 and NOVA2 or miR‐635 was analyzed by dual‐luciferase reporter assay and RNA immunoprecipitation (RIP) assay. An in vivo transplanted tumor model was established to confirm the effect of circ_0102231 on tumor formation.ResultsCirc_0102231 was abnormally upregulated in NSCLC tissues and correlated with clinical stage. Silencing of circ_0102231 inhibited cell proliferation and angiogenesis but significantly promoted the apoptosis of NSCLC cells. There were target binding sites between circ_0102231 and miR‐635, miR‐635 and NOVA2. Importantly, circ_0102231 acted as a sponge for miR‐635, increased the expression of NOVA2, and activated the PI3K/AKT signaling pathway. Finally, silencing of circ_0102231 also had obvious antitumor effects in vivo.ConclusionCirc_0102231 increased the expression of NOVA2 by interacting with miR‐635 to promote the malignant progression of NSCLC.

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“…Their relationship with tumorigenesis has previously been reported. For example, miR-635 was shown to be a potential inhibiting factor in NSCLC and gastric cancer [17,18]. MiR-668-3p expression was shown to be significantly increased in hepatocellular carcinoma [19].…”

Section: Discussionmentioning

confidence: 99%

Hsa-miR-1248 suppressed the proliferation, invasion and migration of colorectal cancer cells via inhibiting PSMD10

Wang

Liang

et al. 2022

BMC Cancer

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Background Lymph node metastasis (LNM) is a critical event during the colorectal cancer (CRC) development and is indicative of poor prognosis. Identification of molecular markers of LNM may facilitate better therapeutic decision-making. Methods Six pairs of CRC tissues and corresponding adjacent tissues [3 pairs diagnosed as pT1N0M0 (M_Low group) and 3 pairs diagnosed as pT4N2M0 (M_High group)] collected from CRC patients who underwent surgical resection were used. MicroRNA sequencing was performed to screen differential microRNAs involved in CRC LNM. The selected microRNAs were validated in CRC tissues and cell lines using qRT-PCR. The functions of candidate hsa-miR-1248 were evaluated by CCK-8, colony formation, and Transwell assay. The binding of hsa-miR-1248 with its target PSMD10 was confirmed by luciferase activity assay, and the expression of PSMD10 in tissues was detected by droplet digital polymerase chain reaction. Results Ninety-five miRNAs were downregulated in carcinoma tissues (M_Low and M_high groups) compared with the normal group. Their expression in M_High group was significantly lower compared with M_Low group. The top 3 were hsa-miR-635, hsa-miR-1248, and hsa-miR-668-3p. After validation in tissues/cell lines, only hsa- hsa-miR-1248 was decreased in high metastatic tissues or SW620 cells compared to low metastatic tissues or SW480 cells. Hsa-miR-1248 was found to inhibit CRC cell viability, proliferation, invasion, and migration. The tumor suppressor effect of has-miR-1248 in CRC cells was attenuated or enhanced by up-regulating or down-regulating PSMD10, respectively. Conclusion Hsa-miR-1248 may act as a tumor suppressor gene in CRC by targeting and inhibiting PSMD10, which provides a clue for CRC treatment.

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Circ_0000735 enhances the proliferation, metastasis and glycolysis of non-small cell lung cancer by regulating the miR-635/FAM83F axis

Cited by 11 publications

References 27 publications

Blocking circ_0010235 suppresses acquired paclitaxel resistance of non-small cell lung cancer by sponging miR-512-5p to modulate FAM83F expression

Blocking circ_0010235 suppresses acquired paclitaxel resistance of non-small cell lung cancer by sponging miR-512-5p to modulate FAM83F expression

Circ_0102231 inactivates the PI3K/AKT signaling pathway by regulating the miR‐635/NOVA2 pathway to promote the progression of non‐small cell lung cancer

Hsa-miR-1248 suppressed the proliferation, invasion and migration of colorectal cancer cells via inhibiting PSMD10

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