MiR‐148b suppressed non‐small cell lung cancer progression via inhibiting ALCAM through the NF‐κB signaling pathway

Jiang, Zhe; Zhang, Jingwen; Chen, Fuhui; Sun, Yajiao

doi:10.1111/1759-7714.13285

Cited by 20 publications

(12 citation statements)

References 35 publications

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“…These inconsistencies may be due to the differences between sample origins and the tumor clinicopathological characteristics (33); therefore, further research should be conducted in various human cancer types to determine the effect of miR-590-5p. The role of miRNA molecules in lung cancer, such as miR-148b, miR-590-3p and miR-455-5p, has been investigated in previous studies (39)(40)(41). miR-590 has been proposed to act as an oncogene or as a tumor suppressor gene depending on the target (42).…”

Section: Discussionmentioning

confidence: 99%

Knockdown of lncRNA NUTM2A‑AS1 inhibits lung adenocarcinoma cell viability by regulating the miR‑590‑5p/METTL3 axis

2021

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Lung adenocarcinoma (LUAD) is the leading cause of cancer-related mortality worldwide. Long non-coding RNA (lncRNA) NUT family member 2A antisense RNA 1 (NUTM2A-AS1) is dysregulated in LUAD; however, its role in this disease remains unclear. The present study aimed to identify the underlying molecular mechanism of the effect of lncRNA NUTM2A-AS1 in LUAD by exploring whether lncRNA NUTM2A-AS1 could affect LUAD cell proliferation and apoptosis through the microRNA (miR)-590-5p/methyltransferase 3, N6-adenosine-methyltransferase complex catalytic subunit (METTL3) axis. miR-590-5p was predicted and verified as the direct target of NUTM2A-AS1 using bioinformatics analysis and a dual luciferase reporter assay. The expression levels of NUTM2A-AS1 and miR-590-5p in lung cancer cells, and the effects of NUTM2A-AS1 on cell viability and apoptosis were determined using MTT assays and flow cytometry, respectively. Reverse transcription-quantitative PCR analysis revealed that the expression levels of NUTM2A-AS1 were significantly upregulated, while those of miR-590-5p were significantly downregulated, in lung cancer cells compared with the control epithelial cells. NUTM2A-AS1 knockdown inhibited NCI-H23 cell viability and induced apoptosis by upregulating miR-590-5p expression. Moreover, the function and regulatory mechanism of miR-590-5p in LUAD were also investigated. It was determined that miR-590-5p could interact with METTL3, and further analysis of the expression levels of METTL3 in lung cancer cells demonstrated that METTL3 was significantly upregulated in NCI-H23 and A549 cells compared with the control cells. In addition, miR-590-5p inhibited NCI-H23 cell viability and induced apoptosis by downregulating METTL3 expression. In conclusion, the findings of the present study suggested that NUTM2A-AS1 knockdown may inhibit LUAD progression by regulating the miR-590-5p/METTL3 axis. These results may provide insight into the mechanisms underlying the tumorigenesis of LUAD and offer a new treatment strategy for the disease.

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Section: Discussionmentioning

confidence: 99%

Knockdown of lncRNA NUTM2A‑AS1 inhibits lung adenocarcinoma cell viability by regulating the miR‑590‑5p/METTL3 axis

2021

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“…This suggests that miR-148b plays an important role in cancer dynamics, including melanoma. In non-small-cell lung cancer, miR-148b suppresses tumor growth and metastasis by regulating the NF- κ B and MAPK/JNK pathways [ 28 , 29 ]. Leong et al reported that miR-148a/b-3p targets an isoform of RAS-like protein (RALBP1) and thus functions as a tumor suppressor in oral squamous cell carcinomas [ 30 ].…”

Section: Discussionmentioning

confidence: 99%

MicroRNA-148b Inhibits the Malignant Biological Behavior of Melanoma by Reducing Sirtuin 7 Expression Levels

Sun

Guo

Fan

et al. 2020

BioMed Research International

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There is growing evidence that microRNA-148b (miR-148b) can inhibit the growth of malignant cells while sirtuin 7 (SIRT7) may perform its carcinogenic effect by deacetylating H3K18. This study investigated the mechanism of miR-148b/SIRT7 on how it affects the malignant biological behavior of melanoma. It was established that the expression of miR-148b was downregulated in melanoma while that of SIRT7 was upregulated but negatively regulated by miR-148b through binding to the 3 ′ UTR of SIRT7. Ectopic expression of miR-148b reduced the proliferation, migration, and invasion of melanoma cells, but SIRT7 reversed these functions of miR-148b. Moreover, tumor growth and metastasis experiments showed that miR-148b could significantly suppress proliferation and metastasis of melanoma in vivo. Overall, miR-148b inhibits the malignant biological behavior of melanoma by reducing the expression level of SIRT7. The development of miR-148b as a novel potential therapeutic approach for melanoma may be possible in the future.

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“…However, attempts have been conducted in improving knowledge toward genetic factors responsible for the development and progression of these thoracic cancers. MicroRNAs (miRNAs), as non-coding and short RNA molecules, are considered as potential diagnostic, therapeutic, and prognostic factors for breast and lung cancers [ 19 , 20 ]. There are two major types including tumor-suppressor and tumor-promoting miRNAs whose roles in the development of breast and lung cancers have been elucidated [ 21 , 22 , 23 , 24 ].…”

Section: Introductionmentioning

confidence: 99%

Small in Size, but Large in Action: microRNAs as Potential Modulators of PTEN in Breast and Lung Cancers

et al. 2021

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MicroRNAs (miRNAs) are well-known regulators of biological mechanisms with a small size of 19–24 nucleotides and a single-stranded structure. miRNA dysregulation occurs in cancer progression. miRNAs can function as tumor-suppressing or tumor-promoting factors in cancer via regulating molecular pathways. Breast and lung cancers are two malignant thoracic tumors in which the abnormal expression of miRNAs plays a significant role in their development. Phosphatase and tensin homolog (PTEN) is a tumor-suppressor factor that is capable of suppressing the growth, viability, and metastasis of cancer cells via downregulating phosphatidylinositol 3-kinase (PI3K)/protein kinase B (Akt) signaling. PTEN downregulation occurs in lung and breast cancers to promote PI3K/Akt expression, leading to uncontrolled proliferation, metastasis, and their resistance to chemotherapy and radiotherapy. miRNAs as upstream mediators of PTEN can dually induce/inhibit PTEN signaling in affecting the malignant behavior of lung and breast cancer cells. Furthermore, long non-coding RNAs and circular RNAs can regulate the miRNA/PTEN axis in lung and breast cancer cells. It seems that anti-tumor compounds such as baicalein, propofol, and curcumin can induce PTEN upregulation by affecting miRNAs in suppressing breast and lung cancer progression. These topics are discussed in the current review with a focus on molecular pathways.

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MiR‐148b suppressed non‐small cell lung cancer progression via inhibiting ALCAM through the NF‐κB signaling pathway

Cited by 20 publications

References 35 publications

Knockdown of lncRNA NUTM2A‑AS1 inhibits lung adenocarcinoma cell viability by regulating the miR‑590‑5p/METTL3 axis

Knockdown of lncRNA NUTM2A‑AS1 inhibits lung adenocarcinoma cell viability by regulating the miR‑590‑5p/METTL3 axis

MicroRNA-148b Inhibits the Malignant Biological Behavior of Melanoma by Reducing Sirtuin 7 Expression Levels

Small in Size, but Large in Action: microRNAs as Potential Modulators of PTEN in Breast and Lung Cancers

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