NUCKS promotes cell proliferation and suppresses autophagy through the mTOR-Beclin1 pathway in gastric cancer

Zhao, Erhu; Feng, Lin; Bai, Longchang; Cui, Hongjuan

doi:10.1186/s13046-020-01696-7

Cited by 25 publications

(22 citation statements)

References 54 publications

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“…The effects of the PI3K/Akt pathway in cancer cell cycle process, survive, metabolism, motility and the tumor angiogenesis and inflammatory cell recruitment have been well established [23,24]. Some studies have reported that NUCKS regulates gastric cancer cell proliferation and apoptosis though PI3K/AKT/mTOR signalling pathway [7,21]. In the present study, the phosphorylation of PI3K and AKT were suppressed by NUCKS knockdown compared with that in si-NC group in A549 cells.…”

Section: Discussionsupporting

confidence: 48%

“…The chromosomal protein nuclear ubiquitous casein and cyclin-dependent kinases substrate (NUCKS) is a highly phosphorylated protein that is similar to the high-mobility group protein family and is involved in the tumorigenesis of various human malignancies [6,7]. In addition, NUCKS overexpression has been reported in numerous cancers and has been shown to enhance tumor cell viability and invasion [7][8][9]. However, its role in the progression of lung cancer is not well understood.…”

Section: Introductionmentioning

confidence: 99%

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NUCKS Promotes the Proliferation, Migration and Invasion of Lung Cancer Cells Through Pi3k/Akt Signalling Pathway

Zhou

Hua

et al. 2021

CIM

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Purpose: Nuclear ubiquitous casein and cyclin-dependent kinases substrate (NUCKS) overexpression has been reported in various types of cancers. The purpose of this study is to clarify the role of NUCKS, underlying the involvement of non-small-cell lung cancer, in the progression of lung cancer. Methods: The small interfering ribonucleic acid (siRNA) of NUCKS was transfected into a lung cancer cell line (NCI-H460, A549, NCI-H1299 and NCI-H1975). Functional experiments (MTT assay, Annexin V-FITC/PI double staining assay, colony formation assay, wound healing assay and Transwell assay) were performed to measure the effects of NUCKS on lung cancer cell viability, migration, invasion and apoptosis. Results: NUCKS was found to be up-regulated in lung cancer cells. Knockdown of NUCKS significantly altered lung cancer cell apoptosis, proliferation colony formation, invasion and migration. Moreover, knockdown of NUCKS attenuated the activation of the PI3K/AKT pathway in lung cancer cells. Conclusion: NUCKS was overexpressed in lung cancer cells and played an important role in lung cancer by increasing cell growth through the PI3K/AKT signalling pathway. This in vitro study suggested NUCKS should be evaluated in a clinical setting as a novel biomarker and potential therapeutic target for lung cancer.

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Section: Discussionsupporting

confidence: 48%

Section: Introductionmentioning

confidence: 99%

NUCKS Promotes the Proliferation, Migration and Invasion of Lung Cancer Cells Through Pi3k/Akt Signalling Pathway

Zhou

Hua

et al. 2021

CIM

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“…ere is growing evidence that the mTOR signaling pathway plays an important role in the occurrence and development of many malignant cancers [39][40][41][42][43][44], including lung, breast, stomach, and liver cancer. mTOR is a key regulatory factor in the initiation stages of autophagy and functions as a negative regulatory molecule of autophagy, so that its activation inhibits autophagy [45].…”

Section: Discussionmentioning

confidence: 99%

Qiyusanlong Formula Induces Autophagy in Non-Small-Cell Lung Cancer Cells and Xenografts through the mTOR Signaling Pathway

Gao

Wang

Yang

et al. 2021

Evidence-Based Complementary and Alternative Medicine

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Objective. Qiyusanlong (QYSL) formula has been used in the clinic for more than 20 years and has been proved to have pronounced efficacy in the treatment of non-small-cell lung cancer (NSCLC). This work aims to evaluate the molecular mechanism of QYSL formula action on NSCLC, specifically in relation to autophagy induction. Methods. In vitro, CCK-8 was used to detect the effect of QYSL serum on cell viability in A549 cells. In vivo, A549 cells were implanted subcutaneously in nude mice to establish a xenograft model. TUNEL staining was used to measure cell apoptosis and TEM to observe the autophagy-related morphological changes in vitro and in vivo. Western blotting, RT-qPCR, and immunofluorescence were used to measure autophagy-related proteins. In addition, rapamycin (an inhibitor of mTOR and inducer of autophagy) and MHY1485 (an activator of mTOR and inhibitor of autophagy) were used to determine whether QYSL-induced autophagy was regulated by the mTOR pathway. Results. QYSL serum inhibited the cell viability of A549 cells in a concentration‐dependent manner. In vivo, the QYSL formula inhibited xenograft growth. The QYSL formula promoted apoptosis in A549 cells and induced autophagosome formation in vitro and in vivo. In addition, the QYSL formula downregulated the expression of mTOR and p62, while it upregulated the expression of ATG-7 and Beclin-1 and increased the LC3-II/LC3-I ratio. QYSL serum inhibited p-mTOR in a similar manner to rapamycin while reducing the activating effects of MHY1485 on p-mTOR. Conclusion. The QYSL formula has anti-lung cancer effects and promotes autophagy through the mTOR signaling pathway.

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“…Puromycin (2 mg/mL) was used to select successfully transfected cells. Lentiviral production, infection, and establishment of stable human gastric cancer cell lines with the overexpression of the MET gene were performed as previously described [23,24].…”

Section: Transfection and Infectionmentioning

confidence: 99%

Effects of Cynaroside on Cell Proliferation, Apoptosis, Migration and Invasion though the MET/AKT/mTOR Axis in Gastric Cancer

Wang

Sun

et al. 2021

IJMS

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The Chinese medicine monomer cynaroside (Cy) is a flavonoid glycoside compound that widely exists in plants and has a variety of pharmacological effects, such as its important role in the respiratory system, cardiovascular system and central nervous system. Studies have reported that Cy has varying degrees of anticancer activity in non-small cell lung cancer, cervical cancer, liver cancer, esophageal cancer and other cancers. However, there are no relevant reports about its role in gastric cancer. The MET/AKT/mTOR signaling pathway plays important roles in regulating various biological processes, including cell proliferation, apoptosis, autophagy, invasion and tumorigenesis. In this study, we confirmed that Cy can inhibit the cell growth, migration and invasion and tumorigenesis in gastric cancer. Our finding shows that Cy can block the MET/AKT/mTOR axis by decreasing the phosphorylation level of AKT, mTOR and P70S6K. Therefore, the MET/AKT/mTOR axis may be an important target for Cy. In summary, Cy has anti-cancer properties and is expected to be a potential drug for the treatment of gastric cancer.

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NUCKS promotes cell proliferation and suppresses autophagy through the mTOR-Beclin1 pathway in gastric cancer

Cited by 25 publications

References 54 publications

NUCKS Promotes the Proliferation, Migration and Invasion of Lung Cancer Cells Through Pi3k/Akt Signalling Pathway

NUCKS Promotes the Proliferation, Migration and Invasion of Lung Cancer Cells Through Pi3k/Akt Signalling Pathway

Qiyusanlong Formula Induces Autophagy in Non-Small-Cell Lung Cancer Cells and Xenografts through the mTOR Signaling Pathway

Effects of Cynaroside on Cell Proliferation, Apoptosis, Migration and Invasion though the MET/AKT/mTOR Axis in Gastric Cancer

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