Emodin inhibits pancreatic cancer EMT and invasion by up‑regulating microRNA‑1271

Li, Nan; Wang, Chunli; Zhang, Peng; You, Shengyi

doi:10.3892/mmr.2018.9304

Cited by 32 publications

(54 citation statements)

References 36 publications

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“…Several mechanisms have been reported to be involved in the regulation of pancreatic cancer invasion and metastasis, including EMT (32,33). EMT is a process in which cancer cells acquire mesenchymal features and lose epithelial phenotypes at the same time.…”

Section: Discussionmentioning

confidence: 99%

NAF-1 Inhibition by Resveratrol Suppresses Cancer Stem Cell-Like Properties and the Invasion of Pancreatic Cancer

et al. 2020

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Resveratrol is a natural polyphenolic compound with multiple biological effects, e.g., proliferation inhibition, anti-oxidation, and neuroprotection. Besides that, studies have shown that resveratrol inhibits tumor growth and migration, as well as epithelial-mesenchymal transition (EMT). However, its molecular mechanisms in tumor progression are not fully understood. Nutrient-deprivation autophagy factor-1 (NAF-1) is mainly found in the endoplasmic reticulum and mitochondrial outer membrane. It is an important genetic locus for regulating oxidative stress and autophagy. The molecular mechanism of NAF-1 in pancreatic cancer is currently unclear. The current study found that NAF-1 is expressed in pancreatic cancer tissue and correlated with the progression of pancreatic cancer. Furthermore, we found that NAF-1 inhibition significantly inhibits the stem cell characteristics and the invasion and migration abilities of pancreatic cancer cells. In a subcutaneous xenograft model of pancreatic cancer in nude mice, resveratrol inhibited the expression of NAF-1, thereby inhibiting tumor growth. Taken together, resveratrol could be an effective anti-tumor drug, and NAF-1 may be a rational therapeutic target.

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Section: Discussionmentioning

confidence: 99%

NAF-1 Inhibition by Resveratrol Suppresses Cancer Stem Cell-Like Properties and the Invasion of Pancreatic Cancer

et al. 2020

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“…It also induces autophagy to mediate apoptosis through ROS production in human colorectal cancer HCT-116 cells [382]. Moreover, emodin can inhibit tumor growth and metastasis in triple negative breast cancer cells, and human colorectal cancer HCT-116 cells [383,384], whilst it suppresses cell migration and invasion through microRNA-1271 up-regulation in human pancreatic cancer SW1990 cells [385]. In addition, emodin can also inhibit angiogenesis in thyroid and pancreatic cancers [386][387][388].…”

Section: Emodinmentioning

confidence: 99%

Naturally occurring anti-cancer compounds: shining from Chinese herbal medicine

et al. 2019

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Numerous natural products originated from Chinese herbal medicine exhibit anti-cancer activities, including antiproliferative, pro-apoptotic, anti-metastatic, anti-angiogenic effects, as well as regulate autophagy, reverse multidrug resistance, balance immunity, and enhance chemotherapy in vitro and in vivo. To provide new insights into the critical path ahead, we systemically reviewed the most recent advances (reported since 2011) on the key compounds with anti-cancer effects derived from Chinese herbal medicine (curcumin, epigallocatechin gallate, berberine, artemisinin, ginsenoside Rg3, ursolic acid, silibinin, emodin, triptolide, cucurbitacin B, tanshinone I, oridonin, shikonin, gambogic acid, artesunate, wogonin, β-elemene, and cepharanthine) in scientific databases (PubMed, Web of Science, Medline, Scopus, and Clinical Trials). With a broader perspective, we focused on their recently discovered and/or investigated pharmacological effects, novel mechanism of action, relevant clinical studies, and their innovative applications in combined therapy and immunomodulation. In addition, the present review has extended to describe other promising compounds including dihydroartemisinin, ginsenoside Rh2, compound K, cucurbitacins D, E, I, tanshinone IIA and cryptotanshinone in view of their potentials in cancer therapy. Up to now, the evidence about the immunomodulatory effects and clinical trials of natural anti-cancer compounds from Chinese herbal medicine is very limited, and further research is needed to monitor their immunoregulatory effects and explore their mechanisms of action as modulators of immune checkpoints.

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“…In the meantime, other studies have revealed that miR‐1271 had a strong inhibitory effect on tumor cell proliferation and metastasis, for instance, Li et al . found that Emodin could obviously inhibit the epithelial‐mesenchymal transition (EMT) process and cell invasive capacity in pancreatic cancer, which was attributed to the up‐regulated miR‐1271 . Similarly, miR‐1271 had the ability to inhibit cell growth, migration and invasion in gastric cancer through blocking the dual specificity mitogen‐activated protein kinase kinase 1 and TEA domain (TEAD) 4 transcription factor (TEAD4) .…”

Section: Introductionmentioning

confidence: 99%

Effects of microRNA‐1271 on ovarian cancer via inhibition of epithelial‐mesenchymal transition and cisplatin resistance

Chen

Wang

Zhou³

2019

J of Obstet and Gynaecol

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Aim: Efficacy of platinum based-chemotherapy is limited by cisplatin (DDP) resistance, however, the underlying mechanism of cisplatin resistance remains unclear. We aimed to investigate the role of miR-1271 in cisplatin-resistant ovarian cancer cells. Methods: Transfection of miR-1271 mimic and inhibitor was performed to study the role of miR-1271 in ovarian cancer. Cell viability was assessed by Cell Counting Kit (CCK)-8 assay. Flow cytometry was used to determine the apoptosis rates. Quantitative reverse transcription polymerase chain reaction (qRT-PCR) and Western blot were used to detect mRNA and protein expressions. Target predicted by Targetscan7.2 was confirmed by dual-luciferase activity assay. Mammalian target of rapamycin (mTOR) siRNA (simTOR) co-transfection was performed to verify the role of mTOR in the suppression effect of miR-1271 on ovarian cancer. Results: In SKOV3 cells, miR-1271 overexpression significantly decreased cell viability and up-regulated apoptosis rate (from 5.54% of control to 24.03%). MiR-1271 adversely affected SKOV3 cell migration and invasion, and induced the upregulation of E-cadherin and downregulation of N-cadherin and alpha-smooth muscle actin (α-SMA). Moreover, SKOV3/DDP cells had a lower miR-1271 level, and enhancing miR-1271 contributed strongly to cisplatin-induced apoptosis through altering the expressions of B-cell lymphoma-2 associated X protein (BAX), cleaved caspase-3 and B-cell lymphoma 2 (Bcl-2). In contrast, the opposite result was observed in miR-1271 inhibitor. mTOR was identified to be a target of miR-1271. SimTOR partially reversed the increased cell viability under the effect of miR-1271 inhibitor. Conclusion: Our data indicate that miR-1271 can inhibit the ovarian cancer epithelial-mesenchymal transition (EMT) and sensitize resistant cells to cisplatin-induced apoptosis through blocking mTOR expression.

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Emodin inhibits pancreatic cancer EMT and invasion by up‑regulating microRNA‑1271

Cited by 32 publications

References 36 publications

NAF-1 Inhibition by Resveratrol Suppresses Cancer Stem Cell-Like Properties and the Invasion of Pancreatic Cancer

NAF-1 Inhibition by Resveratrol Suppresses Cancer Stem Cell-Like Properties and the Invasion of Pancreatic Cancer

Naturally occurring anti-cancer compounds: shining from Chinese herbal medicine

Effects of microRNA‐1271 on ovarian cancer via inhibition of epithelial‐mesenchymal transition and cisplatin resistance

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