Triptolide reduces proliferation and enhances apoptosis of human non-small cell lung cancer cells through PTEN by targeting miR-21

Li, Xiaofang; Zang, Aimin; Jia, Yongsheng; Zhang, Jinchao; Fan, Wufang; Feng, Jian; Duan, Mindan; Zhang, Lei; Huo, Ran; Jen, Jin; Zhu, Xiaowei

doi:10.3892/mmr.2016.4844

Cited by 36 publications

(28 citation statements)

References 29 publications

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“…Previous studies had shown the roles of tumor-derived miR-21 in multiple steps of tumor progression, including tumor growth at primary and secondary sites, invasion, migration, and extracellular matrix modification. MiR-21 promoted tumor growth by repressing many tumor suppressor genes, including PTEN, 8,9 /CDK2AP1, 15 and B-cell translocation gene-2 (BTG-2), 16 and inhibiting B-cell lymphoma-2 (BCL-2), 17 an apoptosis gene. MiR-21 also increased cell motility and invasion by down-regulation of metastasis-related tumor suppressor genes, including maspin and programmed cell death 4 (PDCD4).…”

Section: Discussionmentioning

confidence: 99%

“…MiR-21 targets PTEN in lung cancer cells and hepatocellular cancer cells to enhance their proliferation and reduce apoptosis. 8,9 Very recently PTEN has been shown to play an important role in osteoclast differentiation. 10,11 To further validate our prediction, we performed another crossculture of peripheral blood monocytes and plasma from lung cancer patients with the intervention of exogenous miR-21 Figure 2 The characteristically higher miR-21 level in the plasma of BM patients.…”

Section: Circulating Mir-21 Affected Pten To Promote Osteoclastogenesismentioning

confidence: 99%

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<p>Lung Cancer Cells Derived Circulating miR-21 Promotes Differentiation of Monocytes into Osteoclasts</p>

Zhao¹,

Liu²,

Xie³

et al. 2020

OTT

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Osteoclastogenesis is a key process in osteolytic bone metastasis (BM). Previous studies indicated that some miRNAs could regulate cancers progression and osteoclastogenesis. Our purpose was to investigate the roles of lung cancer cells-derived circulating miR-21 on osteoclastogenesis and its clinical significance in BM patients. Materials and Methods: The difference of miRNA expression in two lung cancer cell lines SBC-5 (with characteristic BM ability) and SBC-3 (without BM ability) were analyzed by microarray and qRT-PCR. Circulating miR-21 levels of lung cancer patients with or without BM were compared by qRT-PCR. The TRAP staining was used to investigate the effects of conditioned media from lung cancer cell lines or patients' plasma with different miR-21 levels on osteoclastogenesis. ROC curve was used to evaluate the diagnostic performance of circulating miR-21 in BM patients. Results: We found that miR-21 expression was specifically higher in SBC-5 than that in SBC-3 cells. The supernatants of SBC-5 cells with higher-level miR-21 promoted osteoclastogenesis. Moreover, we demonstrated that the circulating miR-21 level was significantly higher in BM patients than that in non-BM patients. The plasma from BM patients with higher-level miR-21 could also promote osteoclastogenesis. Mechanistically, lung cancer cells-derived circulating miR-21 could be transferred into osteoclast precursor cells and promote osteoclastogenesis probably by inhibiting PTEN. Finally, clinical data showed that circulating miR-21 had a potential for the diagnosis of BM. Conclusion: Overall, our findings suggested that circulating miR-21 played important roles in osteoclastogenesis of lung cancer patients and may serve as a biomarker to diagnose BM of lung cancer.

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Section: Discussionmentioning

confidence: 99%

Section: Circulating Mir-21 Affected Pten To Promote Osteoclastogenesismentioning

confidence: 99%

<p>Lung Cancer Cells Derived Circulating miR-21 Promotes Differentiation of Monocytes into Osteoclasts</p>

Zhao¹,

Liu²,

Xie³

et al. 2020

OTT

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“…In particular, miR-21 targets multiple genes in mTOR pathway, including PTEN, p85α and PDCD4. Besides promoting malignant growth, the miR-21/PTEN/PI3K/AKT/mTOR axis has been shown to influence anti-cancer effects of zoledronic acid [80] , triptolide [81] , Metformin [82] , Matrine [83] and curcumin [84] , and modulate radiosensitivity [85, 86] and chemosensitivity to tamoxifen, fulvestrant [87] , sorafenib [88] , cisplatin [89, 90] , imatinib [91] , gefitinib [92] , doxorubicin [93] , daunorubicin [94] , anti-EGFR tyrosine kinase inhibitors (TKI) [95] and the CHOP chemotherapy regimen [96] . miR-21 also influences PI3K/AKT/mTOR signaling via PIK3R1 that negatively regulates p110 subunit under certain circumstances.…”

Section: Mirnas That Activate Mtor Pathwaymentioning

confidence: 99%

Emerging Role of MicroRNAs in mTOR Signaling

Zhang

Huang

Wang³

et al. 2017

Cell. Mol. Life Sci.

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Mechanistic target of rapamycin (mTOR) is a conserved serine/threonine kinase that plays a critical role in the control of cellular growth and metabolism. Hyperactivation of mTOR pathway is common in human cancers, driving uncontrolled proliferation. MicroRNA (miRNA) is a class of short noncoding RNAs that regulate the expression of a wide variety of genes. Deregulation of miRNAs is a hallmark of cancer. Recent studies have revealed interplays between miRNAs and the mTOR pathway during cancer development. Such interactions appear to provide a fine-tuning of various cellular functions and contribute qualitatively to the behavior of cancer. Here we provide an overview of current knowledge regarding the reciprocal relationship between miRNAs and mTOR pathway: regulation of mTOR signaling by miRNAs and control of miRNA biogenesis by mTOR. Further research in this area may prove important for the diagnosis and therapy of human cancer.

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“…The incidence of lung cancer nearly doubled in China over the past ten years. To date, advanced achieve-NAIZHI WANG 1 TAO FENG 1 XIAONA LIU 1 QIN LIU 2, * ment has been made in the treatment of NSCLC. However, many patients with NSCLC are presented with metastasis to existing treatments, such as chemotherapy, radiotherapy and surgery (1).…”

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confidence: 99%

Curcumin inhibits migration and invasion of non-small cell lung cancer cells through up-regulation of miR-206 and suppression of PI3K/AKT/mTOR signaling pathway

et al. 2020

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Curcumin has been proved to inhibit cell proliferation and induce cell apoptosis in non-small cell lung cancer (NSCLC). However, little is known about antimetastatic effects and molecular mechanisms of curcumin in NSCLC. In this study, we investigated the involvement of miR-206 in curcumin’s anti-invasion and anti-migration in NSCLC. Cell proliferation was determined by MTT assay. Cell migration and invasion were analyzed by wound healing assay and transwell assay. MiRNA-206 expression was detected by real-time PCR. Western blot was used to detect the protein expression of PI3K/AKT/mTOR signaling pathway. Curcumin significantly inhibited migration and invasion in A549 cells, accompanied by significantly elevated miR-206 expression. Overexpression of miR-206 could inhibit migration and invasion of A549 cells, but it could also significantly decrease the phosphorylation levels of mTOR and AKT. The inhibition of miR-206 promoted cell migration, invasion and increased the phosphorylation level of mTOR and AKT. Furthermore, miR-206 mimics improved the inhibitory effects of curcumin on cell migration, invasion and the phosphorylation level of mTOR and AKT in A549 cells. On the contrary, MiR-206 inhibitors reversed the inhibitory effects of curcumin on cell migration, invasion and the phosphorylation level of mTOR and AKT. In conclusion, curcumin inhibited cell invasion and migration in NSCLC by elevating the expression of miR-206 which further suppressed the activation of the PI3K/AKT/mTOR pathway.

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Triptolide reduces proliferation and enhances apoptosis of human non-small cell lung cancer cells through PTEN by targeting miR-21

Cited by 36 publications

References 29 publications

<p>Lung Cancer Cells Derived Circulating miR-21 Promotes Differentiation of Monocytes into Osteoclasts</p>

<p>Lung Cancer Cells Derived Circulating miR-21 Promotes Differentiation of Monocytes into Osteoclasts</p>

Emerging Role of MicroRNAs in mTOR Signaling

Curcumin inhibits migration and invasion of non-small cell lung cancer cells through up-regulation of miR-206 and suppression of PI3K/AKT/mTOR signaling pathway

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