&lt;p&gt;LncRNA LINC00461 Promotes Colorectal Cancer Progression via miRNA-323b-3p/NFIB Axis&lt;/p&gt;

Yu, Hairong; Ma, Jun; Chen, Jianshuang; Yang, Yang; Liang, Jianjing; Liang, Yulong

doi:10.2147/ott.s228798

Cited by 18 publications

(8 citation statements)

References 32 publications

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“…Mounting evidence has confirmed that miRNAs could target certain mRNAs and further regulate the development of serious diseases [31][32][33]. To further clarify the effect of miR-486-3p on lung cancer cells, bioinformatics and luciferase reporter assays were applied.…”

Section: Discussionmentioning

confidence: 99%

Circular RNA FLNA acts as a sponge of miR-486-3p in promoting lung cancer progression via regulating XRCC1 and CYP1A1

et al. 2021

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Significantly high-expressed circFLNA has been found in various cancer cell lines, but not in lung cancer. Therefore, this study aimed to explore the role of circFLNA in the progression of lung cancer. The target gene of circFLNA was determined by bioinformatics and luciferase reporter assay. Viability, proliferation, migration, and invasion of the transfected cells were detected by CCK-8, colony formation, wound-healing, and transwell assays, respectively. A mouse subcutaneous xenotransplanted tumor model was established, and the expressions of circFLNA, miR-486-3p, XRCC1, CYP1A1, and related genes in the cancer cells and tissues were detected by RT-qPCR, Western blot, or immunohistochemistry. The current study found that miR-486-3p was low-expressed in lung cancer. MiR-486-3p, which has been found to target XRCC1 and CYP1A1, was regulated by circFLNA. CircFLNA was located in the cytoplasm and had a high expression in lung cancer cells. Cancer cell viability, proliferation, migration, and invasion were promoted by overexpressed circFLNA, XRCC1, and CYP1A1 but inhibited by miR-486-3p mimic and circFLNA knockdown. The weight of the xenotransplanted tumor was increased by circFLNA overexpression yet reduced by miR-486-3p mimic. Furthermore, miR-486-3p mimic reversed the effect of circFLNA overexpression on promoting lung cancer cells and tumors and regulating the expressions of miR-486-3p, XRCC1, CYP1A1, and metastasis/apoptosis/proliferation-related factors. However, overexpressed XRCC1 and CYP1A1 reversed the inhibitory effect of miR-486-3p mimic on cancer cells and tumors. In conclusion, circFLNA acted as a sponge of miR-486-3p to promote the proliferation, migration, and invasion of lung cancer cells in vitro and in vivo by regulating XRCC1 and CYP1A1.

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Section: Discussionmentioning

confidence: 99%

Circular RNA FLNA acts as a sponge of miR-486-3p in promoting lung cancer progression via regulating XRCC1 and CYP1A1

et al. 2021

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“…In recent years, several studies have reported the tumor-related function of LINC00461 in various tumors. For instance, LINC00461 was shown to strengthen the colorectal cancer cells' proliferation and invasion ability by miRNA-323b-3p/NFIB Axis [ 25 ]. LINC00461 was reported to be highly expressed in lung tumor, and its knockdown suppressed the tumor cells' proliferation and metastasis via miR-4478/E2F1 [ 26 ].…”

Section: Discussionmentioning

confidence: 99%

Identification of the 7-lncRNA Signature as a Prognostic Biomarker for Acute Myeloid Leukemia

Liu

Guo

et al. 2021

Disease Markers

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A lot of evidence has emphasized the function of long noncoding RNAs (lncRNAs) in tumors’ development and progression. Nevertheless, there is still a lack of lncRNA biomarkers that can predict the prognosis of acute myeloid leukemia (AML). Our goal was to develop a lncRNA marker with prognostic value for the survival of AML. AML patients’ RNA sequencing data as well as clinical characteristics were obtained from the public TARGET database. Then, differentially expressed lncRNAs were identified in female and male AML samples. By adopting univariate and multivariate Cox regression analyses, AML patients’ survival was predicted by a seven-lncRNA signature. It was found that 95 abnormal expressed lncRNAs existed in AML. Then, the analysis of multivariate Cox regression showed that, among them, 7 (LINC00461, RP11-309M23.1, AC016735.2, RP11-61I13.3, KIAA0087, RORB-AS1, and AC012354.6) had an obvious prognostic value, and according to their cumulative risk scores, these 7 lncRNA signatures could independently predict the AML patients’ overall survival. Overall, the prognosis of AML patients could be predicted by a reliable tool, that is, seven-lncRNA prognostic signature.

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“…However, upstream mediators are able to affect the STAT3/EMT axis. Nuclear factor I/B (NFIB) participates in normal somatic development and recent studies have revealed its role in cancer progression and development [256,257]. NFIB is able to induce Akt phosphorylation.…”

Section: Other Molecular Signaling Pathways Regulate Stat3mentioning

confidence: 99%

STAT3 Pathway in Gastric Cancer: Signaling, Therapeutic Targeting and Future Prospects

Ashrafizadeh

Zarrabi

Orouei

et al. 2020

Biology

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Molecular signaling pathways play a significant role in the regulation of biological mechanisms, and their abnormal expression can provide the conditions for cancer development. The signal transducer and activator of transcription 3 (STAT3) is a key member of the STAT proteins and its oncogene role in cancer has been shown. STAT3 is able to promote the proliferation and invasion of cancer cells and induces chemoresistance. Different downstream targets of STAT3 have been identified in cancer and it has also been shown that microRNA (miR), long non-coding RNA (lncRNA) and other molecular pathways are able to function as upstream mediators of STAT3 in cancer. In the present review, we focus on the role and regulation of STAT3 in gastric cancer (GC). miRs and lncRNAs are considered as potential upstream mediators of STAT3 and they are able to affect STAT3 expression in exerting their oncogene or onco-suppressor role in GC cells. Anti-tumor compounds suppress the STAT3 signaling pathway to restrict the proliferation and malignant behavior of GC cells. Other molecular pathways, such as sirtuin, stathmin and so on, can act as upstream mediators of STAT3 in GC. Notably, the components of the tumor microenvironment that are capable of targeting STAT3 in GC, such as fibroblasts and macrophages, are discussed in this review. Finally, we demonstrate that STAT3 can target oncogene factors to enhance the proliferation and metastasis of GC cells.

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<p>LncRNA LINC00461 Promotes Colorectal Cancer Progression via miRNA-323b-3p/NFIB Axis</p>

Cited by 18 publications

References 32 publications

Circular RNA FLNA acts as a sponge of miR-486-3p in promoting lung cancer progression via regulating XRCC1 and CYP1A1

Circular RNA FLNA acts as a sponge of miR-486-3p in promoting lung cancer progression via regulating XRCC1 and CYP1A1

Identification of the 7-lncRNA Signature as a Prognostic Biomarker for Acute Myeloid Leukemia

STAT3 Pathway in Gastric Cancer: Signaling, Therapeutic Targeting and Future Prospects

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