MicroRNA‐1 overexpression increases chemosensitivity of non‐small cell lung cancer cells by inhibiting autophagy related 3‐mediated autophagy

Li, Hua; Zhu, Guirong; Wei, Jianguo

doi:10.1002/cbin.10995

Cited by 52 publications

(27 citation statements)

References 35 publications

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“…indeed, the data from the present study showed that paclitaxeland ddP-induced apoptosis was increased in Bc cells that overexpressed mir-1. Similar the current study, Hua et al (31) reported that mir-1 overexpression improved ddP sensitivity by inhibiting aTG3-mediated autophagy in non-small cell lung cancer cells. Thus, mir-1 may have a role in the treatment of Bc patients who are administered paclitaxel and ddP, but the specific mechanism requires further investigation in the future.…”

Section: Discussionsupporting

confidence: 89%

Upregulation of microRNA‑1 inhibits proliferation and metastasis of breast cancer

Peng

Yuan

et al. 2020

Mol Med Rep

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recent studies have shown that micrornas (mirs) play a key role in the regulation of cancer development. in the present study, reverse transcription-quantitative Pcr was used to detect the expression of mir-1 in breast cancer and adjacent tissues, and survival analysis was performed to compare the low-expression groups with the Kaplan-Meier method. overexpression of mir-1 was used to observe the effects on the proliferation, migration and invasion of breast cancer cells in vitro and in vivo. Moreover, Bcl-2 expression was measured by western blotting and luciferase assays after the overexpression of mir-1. The present study reported that mir-1 is expressed at low levels in breast cancer and that cell proliferation, migration and invasion are inhibited in mir-1-overexpressing cells. enhanced mir-1 expression can also increase cell apoptosis. The present study also demonstrated that Bcl-2 is a potential target of mir-1. In vivo studies indicate that overexpression of mir-1 decreases tumor volume and weight in nude mice. The data from the present study demonstrated for the first time that overexpression of mir-1 increases the sensitivity of breast cancer cells to paclitaxel and cisplatin. The present study provided new evidence for the important role of mir-1 in the tumorigenesis and drug sensitivity of breast cancer.

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Section: Discussionsupporting

confidence: 89%

Upregulation of microRNA‑1 inhibits proliferation and metastasis of breast cancer

Peng

Yuan

et al. 2020

Mol Med Rep

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“…Subsequent promotion of cell survival can be inhibited by knockdown of Atg5, an important regulator of autophagosome formation (46,47,55). Evidence further suggests a protective role for autophagy regulators ATG3, 5, 6, 7, and 12 in resistant cells, however, detailed mechanisms are not yet fully understood and hence require further studies (56)(57)(58)(59)(60). Interestingly, besides TFEB-regulated lysosomal alterations upon treatment with cytostatics, TFEB also contributes to cell survival by mechanisms independent of the aforementioned.…”

Section: Tfeb Signaling Regulating Drug Resistancementioning

confidence: 99%

Targeting Lysosomes in Cancer as Promising Strategy to Overcome Chemoresistance—A Mini Review

et al. 2020

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To date, cancer remains a worldwide leading cause of death, with a still rising incidence. This is essentially caused by the fact, that despite the abundance of therapeutic targets and treatment strategies, insufficient response and multidrug resistance frequently occur. Underlying mechanisms are multifaceted and extensively studied. In recent research, it became evident, that the lysosome is of importance in drug resistance phenotypes. While it has long been considered just as cellular waste bag, it is now widely known that lysosomes play an important role in important cellular signaling processes and are in the focus of cancer research. In that regard lysosomes are now considered as so-called "drug safe-houses" in which chemotherapeutics are trapped passively by diffusion or actively by lysosomal P-glycoprotein activity, which prevents them from reaching their intracellular targets. Furthermore, alterations in lysosome to nucleus signaling by the transcription factor EB (TFEB)-mTORC1 axis are implicated in development of chemoresistance. The identification of lysosomes as essential players in drug resistance has introduced novel strategies to overcome chemoresistance and led to innovate therapeutic approaches. This mini review gives an overview of the current state of research on the role of lysosomes in chemoresistance, summarizing underlying mechanisms and treatment strategies and critically discussing open questions and drawbacks.

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“…Recently, the regulation of autophagy by miR-NAs has been shown to be a potentially effective strategy to reduce cancer cell chemoresistance [34]. Regarding NSCLC, while some studies have revealed a potential role of miRNAs and autophagy in cisplatin resistance in NSCLC [35,36], no investigations have verified the ability of miR-223 and FBXW7 to directly impact the regulation of autophagy and cisplatin resistance in NSCLC cells. Therefore, additional studies are required to elucidate the relationship between miRNAs, autophagy, and cisplatin resistance in NSCLC.…”

Section: Discussionmentioning

confidence: 99%

MiR-223 regulates autophagy associated with cisplatin resistance by targeting FBXW7 in human non-small cell lung cancer

et al. 2020

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Background: Cisplatin is widely used as a first-line treatment for non-small cell lung cancer (NSCLC), but chemoresistance remains a major clinical obstacle for efficient use. As a microRNA, miR-223 was reported to promote the doxorubicin resistance of NSCLC. However, whether miR-223 is also involved in cisplatin resistance of NSCLC and the mechanism miR-223 involved in drug resistance is unclear. Accumulated evidence has shown that abnormal autophagy is associated with tumor chemoresistance. The study aimed to study the role of miR-223 on cisplatin sensitivity in NSCLC and uncover the potential mechanisms. Methods: NSCLC cells transfected with mimic or inhibitor for miR-223 was assayed for chemoresistance in vitro. MiR-223 expression was assessed by quantitative real-time PCR (qRT-PCR). Western blot were used to study the expression level of F-box/WD repeat-containing protein 7 (FBXW7) and autophagy-related protein. The effect of miR-223 on cisplatin sensitivity was examined by using CCK-8, EdU assays and Autophagic flux assay. Luciferase assays, EdU assays and small interfering RNA were performed to identify the targets of miR-223 and the mechanism by which it promotes treatment resistance. Xenograft models were established to investigate the effect of mir-223 on cisplatin sensitivity. Results: In the present study, we found that the level of miR-223 was significantly positively correlated with cisplatin resistance. MiR-223 overexpression made NSCLC cells resistant to cisplatin treatment. We further found that autophagy mediated miR-223-mediated cisplatin resistance in NSCLC cells. Further mechanistic research demonstrated that miR-223 directly targeted FBXW7. The overexpression of miR-223 could inhibit the level of FBXW7 protein expression, thus promoting autophagy and making NSCLC cells resistant to cisplatin. Finally, we confirmed the increased effect of cisplatin sensitivity by miR-223 Antagomir in xenograft models of NSCLC. Conclusions: Our results demonstrate that miR-223 could enhance autophagy by targeting FBXW7 in NSCLC cells. Inhibition of autophagy by miR-223 knockdown provides a novel treatment strategy to alleviate cisplatin resistance in NSCLC.

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MicroRNA‐1 overexpression increases chemosensitivity of non‐small cell lung cancer cells by inhibiting autophagy related 3‐mediated autophagy

Cited by 52 publications

References 35 publications

Upregulation of microRNA‑1 inhibits proliferation and metastasis of breast cancer

Upregulation of microRNA‑1 inhibits proliferation and metastasis of breast cancer

Targeting Lysosomes in Cancer as Promising Strategy to Overcome Chemoresistance—A Mini Review

MiR-223 regulates autophagy associated with cisplatin resistance by targeting FBXW7 in human non-small cell lung cancer

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