Echinacoside inhibits hepatocellular carcinoma progression by targeting the miR-30c-5p/FOXD1/KLF12 axis.

BACKGROUND: Hepatocellular carcinoma (HCC) is the third leading cause of cancer-attributed mortality and the primary liver malignancy in the world. Echinacoside is a phenylethanoid glycoside derived from traditional Chinese medicinal herbs which possessed multiple health benefits on humans, including anti-tumor effects. OBJECTIVE: This study aimed to demonstrate the function of echinacoside in HCC progression and the involvement of miR-30c-5p/FOXD1/KLF12 axis. METHODS: The HepG2 cells were treated by different dose of echinacoside, miR-30c-5p mimic, miR-30c-5p inhibitor, and FOXD1 overexpression lentiviruses or siRNA individually or simultaneously. The cell invasion and migration were measured by transwell assay. RNA and protein levels were tested by RT-PCR and western blot, respectively. The regulatory function of miR-30c-5p on Forkhead box D1 (FOXD1), FOXD1 on Krüppel-like factor 12 (KLF12) was tested by luciferase reporter assay or/and ChIP assay. Meanwhile, a liver cancer lung metastasis mice model was used to examine the functions of echinacoside and miR-30c-5p on HCC metastasis in vivo. Moreover, the correlations among miR-30c-5p, FOXD1, KLF12, and HCC prognosis was analyzed using clinical sample and TCGA database. RESULTS: Based on both in vitro and in vivo investigations, we found that echinacoside could inhibit HCC cell migration, invasiveness, and tumor metastasis, and associated with the enhanced miR-30c-5p/FOXD1/KLF12 axis. Furthermore, through analyzing the interactions among intermediate molecules, we revealed that miR-30c-5p, FOXD1, and KLF12üere clinically relevant with each other in HCC patients, correlated with HCC prognosis, and regulated by echinacoside to contribute in the inhibition of HCC progression. CONCLUSIONS: These findings suggest that echinacoside could inhibit HCC progression, and the mechanism related to the enhanced miR-30c-5p/FOXD1/KLF12 axis. Moreover, the abovementioned intermediate molecules might serve as prospective biomarkers for HCC prognosis.

Applications of CT-based radiomics for the prediction of immune checkpoint markers and immunotherapeutic outcomes in non-small cell lung cancer.

In recent years, there has been significant research interest in the field of immunotherapy for non-small cell lung cancer (NSCLC) within the academic community. Given the observed variations in individual responses, despite similarities in histopathologic type, immunohistochemical index, TNM stage, or mutation status, the identification of a reliable biomarker for early prediction of therapeutic responses is of utmost importance. Conventional medical imaging techniques primarily focus on macroscopic tumor monitoring, which may no longer adequately fulfill the requirements of clinical diagnosis and treatment. CT (computerized tomography) or PEF/CT-based radiomics has the potential to investigate the molecular-level biological attributes of tumors, such as PD-1/PD-L1 expression and tumor mutation burden, which offers a novel approach to assess the effectiveness of immunotherapy and forecast patient prognosis. The utilization of cutting-edge radiological imaging techniques, including radiomics, PET/CT, machine learning, and artificial intelligence, demonstrates significant potential in predicting diagnosis, treatment response, immunosuppressive characteristics, and immune-related adverse events. The current review highlights that CT scan-based radiomics is a reliable and feasible way to predict the benefits of immunotherapy in patients with advanced NSCLC.

[Retracted] MicroRNA­584 prohibits hepatocellular carcinoma cell proliferation and invasion by directly targeting BDNF.

Following the publication of this paper, it was drawn to the Editor's attention by a concerned reader that the Transwell invasion assay data shown in Fig. 2C and D on p. 1997 were strikingly similar to data appearing in different form in other articles written by different authors at different research institutes that had either already been published, or were submitted for publication at around the same time (and in some cases, have subsequently been retracted).  Owing to the fact that the contentious data in the above article had already been published prior to its submission to Molecular Medicine Reports, the Editor has decided that this paper should be retracted from the Journal. The authors were asked for an explanation to account for these concerns, but the Editorial Office did not receive a  reply. The Editor apologizes to the readership for any inconvenience caused. [Molecular Medicine Reports  20: 1994-2001, 2019; DOI: 10.3892/mmr.2019.10424].

X-ray Activated Nanoprodrug for Visualization of Cortical Microvascular Alterations and NIR-II Image-Guided Chemo-Radiotherapy of Glioblastoma.

The permeability of the highly selective blood-brain barrier (BBB) to anticancer drugs and the difficulties in defining deep tumor boundaries often reduce the effectiveness of glioma treatment. Thus, exploring the combination of multiple treatment modalities under the guidance of second-generation near-infrared (NIR-II) window fluorescence (FL) imaging is considered a strategic approach in glioma theranostics. Herein, a hybrid X-ray-activated nanoprodrug was developed to precisely visualize the structural features of glioma microvasculature and delineate the boundary of glioma for synergistic chemo-radiotherapy. The nanoprodrug comprised down-converted nanoparticle (DCNP) coated with X-ray sensitive poly(Se-Se/DOX-co-acrylic acid) and targeted Angiopep-2 peptide (DCNP@P(Se-DOX)@ANG). Because of its ultrasmall size and the presence of DOX, the nanoprodrug could easily cross BBB to precisely monitor and localize glioblastoma via intracranial NIR-II FL imaging and synergistically administer antiglioblastoma chemo-radiotherapy through specific X-ray-induced DOX release and radiosensitization. This study provides a novel and effective strategy for glioblastoma imaging and chemo-radiotherapy.

Genome-wide DNA methylation analysis of Astragalus and Danshen on the intervention of myofibroblast activation in idiopathic pulmonary fibrosis.

BACKGROUND: Idiopathic pulmonary fibrosis (IPF), a chronic progressive interstitial lung disease of unknown etiology, is characterized by continuous damage to alveolar epithelial cells, abnormal repair of alveolar tissue, and alveolar wall scar formation. Currently, the recommended treatment for IPF in Western medicine is relatively limited. In contrast, traditional Chinese medicine and compound prescriptions show advantages in the diagnosis and treatment of IPF, which can be attributed to their multi-channel and multi-target characteristics and minimal side-effects. The purpose of this study was to further corroborate the effectiveness and significance of the traditional Chinese medications Astragalus and Danshen in IPF treatment. METHODS: We performed whole-genome methylation analysis on nine rat lung tissue samples to determine the epigenetic variation between IPF and non-fibrotic lungs using Gene Ontology and Kyoto Encyclopedia of Genes and Genomes pathway enrichment analyses and quantitative reverse transcription polymerase chain reactions. RESULTS: We identified differentially methylated regions and 105 associated key functional genes in samples related to IPF and Chinese medicine treatment. Based on the methylation levels and gene expression profiles between the Chinese medicine intervention and pulmonary fibrosis model groups, we speculated that Astragalus and Salvia miltiorrhiza (traditionally known as Danshen) act on the Isl1, forkhead box O3, and Sonic hedgehog genes via regulation at transcriptional and epigenetic levels during IPF. CONCLUSIONS: These findings provide novel insights into the epigenetic regulation of IPF, indicate the effectiveness of Astragalus and Danshen in treating IPF, and suggest several promising therapeutic targets for preventing and treating IPF.

A novel necroptosis related gene signature and regulatory network for overall survival prediction in lung adenocarcinoma.

We downloaded the mRNA expression profiles of patients with LUAD and corresponding clinical data from The Cancer Genome Atlas (TCGA) database and used the Least Absolute Shrinkage and Selection Operator Cox regression model to construct a multigene signature in the TCGA cohort, which was validated with patient data from the GEO cohort. Results showed differences in the expression levels of 120 necroptosis-related genes between normal and tumor tissues. An eight-gene signature (CYLD, FADD, H2AX, RBCK1, PPIA, PPID, VDAC1, and VDAC2) was constructed through univariate Cox regression, and patients were divided into two risk groups. The overall survival of patients in the high-risk group was significantly lower than of the patients in the low-risk group in the TCGA and GEO cohorts, indicating that the signature has a good predictive effect. The time-ROC curves revealed that the signature had a reliable predictive role in both the TCGA and GEO cohorts. Enrichment analysis showed that differential genes in the risk subgroups were associated with tumor immunity and antitumor drug sensitivity. We then constructed an mRNA-miRNA-lncRNA regulatory network, which identified lncRNA AL590666. 2/let-7c-5p/PPIA as a regulatory axis for LUAD. Real-time quantitative PCR (RT-qPCR) was used to validate the expression of the 8-gene signature. In conclusion, necroptosis-related genes are important factors for predicting the prognosis of LUAD and potential therapeutic targets.

BreastDM: A DCE-MRI dataset for breast tumor image segmentation and classification.

Dynamic contrast-enhanced magnetic resonance imaging (DCE-MRI) has shown high sensitivity to diagnose breast cancer. However, few computer-aided algorithms focus on employing DCE-MR images for breast cancer diagnosis due to the lack of publicly available DCE-MRI datasets. To address this issue, our work releases a new DCE-MRI dataset called BreastDM for breast tumor segmentation and classification. In particular, a dataset of 232 patients selected with DCE-MR images for benign and malignant cases is established. Each case consists of three types of sequences: pre-contrast, post-contrast, and subtraction sequences. To show the difficulty of breast DCE-MRI tumor image segmentation and classification tasks, benchmarks are achieved by state-of-the-art image segmentation and classification algorithms, including conventional hand-crafted based methods and recently-emerged deep learning-based methods. More importantly, a local-global cross attention fusion network (LG-CAFN) is proposed to further improve the performance of breast tumor images classification. Specifically, LG-CAFN achieved the highest accuracy (88.20%, 83.93%) and AUC value (0.9154,0.8826) in both groups of experiments. Extensive experiments are conducted to present strong baselines based on various typical image segmentation and classification algorithms. Experiment results also demonstrate the superiority of the proposed LG-CAFN to other breast tumor images classification methods. The related dataset and evaluation codes are publicly available at smallboy-code/Breast-cancer-dataset.

Network pharmacology and molecular docking to explore the pharmacological mechanism of Yifei Tongluo granules in treating idiopathic pulmonary fibrosis: A review.

Idiopathic pulmonary fibrosis (IPF) is an interstitial lung disease that leads to progressive dyspnea and dry cough, with extracellular matrix deposition as the main pathological feature. Yifei Tongluo granules (YTG) are a traditional Chinese medicine formula that could nourish Qi-Yin, clear phlegm, and invigorate blood circulation. In this research, network pharmacology and molecular docking were used to elucidate the potential mechanism of YTG for treating IPF. A total of 278 biologically active compounds were included in YTG, and 16 compounds were selected for pharmacological analysis and molecular docking through "drugs-compounds-intersecting targets of YTG and IPF" network construction. Protein-protein interaction network was constructed using 330 YTG-IPF intersecting targets. Furthermore, Gene Ontology and Kyoto Encyclopedia of Genes and Genomes pathway enrichment analysis were performed. A total of 10 core targets were screened by protein-protein interaction, and molecular docking was used to further validate the binding ability of the compounds to the core targets. The network pharmacology and molecular docking results showed that Danshenol A, isorhamnetin, Ginsenoside-Rh4, quercetin, and kaempferol might be the main active compounds in the treatment of IPF by YTG, whereas MAPK1, MAPK3, EGFR, and SRC are the core targets while PI3K/AKT pathway and MAPK pathway are the main signaling pathways through which YTG regulates relevant biological processes to intervene in IPF. This study shows that YTG can treat IPF by inhibiting the epithelial-mesenchymal transit process, fibroblast proliferation, fibroblast-to-myofibroblast conversion, myofibroblast anti-apoptosis, collagen expression, and other mechanisms.YTG can be widely used as an adjuvant therapy for IPF in clinical practice, and this study provides the basis for subsequent experimental studies.

Curcumin Increases Radiosensitivity of Radioresistant Nasopharyngeal Cancer.

OBJECTIVES: To study the effects of curcumin on the proliferation, invasion, apoptosis, and radiosensitivity of the radioresistant nasopharyngeal carcinoma (NPC) C6661-IR strain as well as the potential radiosensitization mechanism. METHODS: NPC cells were continuously irradiated with different intensities of radiation to induce radiation-resistant cell lines. A plate clone formation assay was used to evaluate the effect of curcumin on the radiosensitivity of NPC cells. 3-(4,5-Dimethylthiazol-2yl)-2,5-diphenyltetrazolium bromide thiazolyl blue (MTT) assay was conducted to detect changes in cell viability. Flow cytometry was employed to analyze apoptosis percentage as well as Transwell® assay and immunofluorescence assay to observe cell invasion. Western blotting was applied to detect the expression levels of Bax, Bcl-2, and pro/cleaved-caspase 3. MiR-205-5p mimics and si-TP53INP1 were synthesized and transfected into C6661-IR cells, and the cells were then incubated with 10 µm/L curcumin. Real-time quantitative reverse transcription PCR (RT-qPCR) was used to measure miR-205-5p levels and western blotting was conducted to detect the expression of TP53INP1. RESULTS: The optimal radiation dose of X-ray was 6 Gy, and this dose was used in all subsequent experiments. Curcumin treatment significantly inhibited the proliferation and invasion of C6661-IR cells, promoted apoptosis and enhanced radiosensitivity. Compared to the 0 Gy+Cur group and the 6 Gy+Cur group, the miR-205-5p levels were higher in the C6661-IR cells of the 0 Gy and 6 Gy groups. Moreover, miR-204-5p was found to directly target TP53INP1. Curcumin downregulated miR-205-5p levels and upregulated TP53INP1 expression (p < 0.05). Thus, modulation of miR-205-5p or TP53INP1 expression attenuates the biological effects of curcumin on C6661-IR cells. CONCLUSIONS: Curcumin inhibited the proliferation and invasion of C6661-IR, promoted apoptosis, and enhanced its radiosensitivity to X-rays by mediating miR-205-5p/TP53INP1 expression.

lncRNA miR4458HG modulates hepatocellular carcinoma progression by activating m6A-dependent glycolysis and promoting the polarization of tumor-associated macrophages.

Long non-coding RNAs (lncRNAs) play significant roles in different biological functions of cancers. However, their function in the metabolism of glucose in patients with human hepatocellular carcinoma (HCC) remains largely unknown. In this study, HCC and paired intact liver tissues were utilized to examine the miR4458HG expression using qRT-PCR and human HCC cell lines to examine cell proliferation, colony formation, and glycolysis after transfection of siRNAs targeting miR4458HG or miR4458HG vectors. The molecular mechanism of miR4458HG was clarified through in situ hybridization, Western blotting, qRT-PCR, RNA pull-down, and RNA immunoprecipitation analysis. The results showed that the miR4458HG affected HCC cell proliferation, activated the glycolysis pathway, and promoted the polarization of tumor-associated macrophage in vitro and in vivo models. Mechanistically, miR4458HG bound IGF2BP2 (a key RNA m6A reader) and facilitated IGF2BP2-mediated target mRNA stability, including HK2 and SLC2A1 (GLUT1), and consequently altered HCC glycolysis and tumor cell physiology. At the same time, HCC-derived miR4458HG could be wrapped in the exosomes and promoted the polarization of tumor-associated macrophage by increasing ARG1 expression. Hence, miR4458HG is oncogenic in nature among patients with HCC. To develop an effective treatment strategy of HCC patients presenting with high glucose metabolism, physicians should focus on miR4458HG and its pathway.

Rxrs and their partner receptor genes inducing masculinization plausibly mediated by endocrine disruption in Paralichthys olivaceus.

Retinoid X receptors (RXRs) can form homo- or heterodimers with orphan receptors involved in multiple intertwined signaling pathways. However, there is limited study on the formation of sex phenotypes and the regulation of steroidogenesis by RXRs in fish. Here, in Paralichthys olivaceus, we first indicated that PPARγ::RXRα was predictably a transcription factor for steroidogenesis genes, and Foxl2 and Dmrt1 were also transcription factors for rxrs and their partner receptor genes. When the flounder fry were exposed to LG100268 (LG, RXRs agonist, 50 mg/kg diet), the percentage of males increased from 50% to 71.4%. Before histological differentiation of the flounder ovary (3 cm TL) and testis (6 cm TL), the transcripts of rar ß and rar γ (P < 0.05) were activated, and the steroidogenesis gene Hsd3b1 was down-regulated (P < 0.05). The ratios of testosterone (T)/17ß-estradiol (E2) were all greatly increased (P < 0.05), and the ratio of 11-ketotestosterone (11-KT)/E2 was elevated at 3 cm TL. Moreover, LG was used to treat the cultured gonads in vitro (10 µM) and the fish with intraperitoneal injection in vivo (12 mg/kg body weight), respectively. LG was able to up-regulate rxr γ, rar γ, and ppar δ, and Hsd3b1 was significantly up-regulated (P < 0.05). The ratios of 11-KT/E2 in the culture medium and in the ovaries of the fish were decreased. Furthermore, the recombinant flounder Foxl2 protein was able to significantly down-regulate ppar γ (P < 0.05) and tr ß (P < 0.01) in the ovaries in vitro, and the result of the Dmrt1 in the testes was opposite to that of the Foxl2, probably indicating a feedback loop between RXRs' partner receptors and Foxl2/Dmrt1. These findings introduce for the first time the mode of action of RXRs on the flounder steroidogenesis and provide important data to learn the potential function of RXRs in fish sex differentiation and the potential role of RXRs in aquatic animals in the presence of water pollutants.

[Retracted] MicroRNA­601 serves as a potential tumor suppressor in hepatocellular carcinoma by directly targeting PIK3R3.

Following the publication of this paper, it was drawn to the Editors' attention by a concerned reader that one of the data panels shown for the cell invasion assays in Fig. 2D was strikingly similar to another data panel that had appeared in different form in another article by different authors. Owing to the fact that the contentious data in the above article had already been published elsewhere prior to its submission to Molecular Medicine Reports, the Editor has decided that this paper should be retracted from the Journal. The authors were asked for an explanation to account for these concerns, but the Editorial Office did not receive a reply. The Editor apologizes to the readership for any inconvenience caused. [Molecular Medicine Reports 19: 2431­2439, 2019; DOI: 10.3892/mmr.2019.9857].

GCHA-Net: Global context and hybrid attention network for automatic liver segmentation.

Liver segmentation is a critical step in liver cancer diagnosis and surgical planning. The U-Net's architecture is one of the most efficient deep networks for medical image segmentation. However, the continuous downsampling operators in U-Net causes the loss of spatial information. To solve these problems, we propose a global context and hybrid attention network, called GCHA-Net, to adaptive capture the structural and detailed features. To capture the global features, a global attention module (GAM) is designed to model the channel and positional dimensions of the interdependencies. To capture the local features, a feature aggregation module (FAM) is designed, where a local attention module (LAM) is proposed to capture the spatial information. LAM can make our model focus on the local liver regions and suppress irrelevant information. The experimental results on the dataset LiTS2017 show that the dice per case (DPC) value and dice global (DG) value of liver were 96.5% and 96.9%, respectively. Compared with the state-of-the-art models, our model has superior performance in liver segmentation. Meanwhile, we test the experiment results on the 3Dircadb dataset, and it shows our model can obtain the highest accuracy compared with the closely related models. From these results, it can been seen that the proposed model can effectively capture the global context information and build the correlation between different convolutional layers. The code is available at the website: https://github.com/HuaxiangLiu/GCAU-Net.

Targeting UBR5 in hepatocellular carcinoma cells and precise treatment via echinacoside nanodelivery.

BACKGROUND: Hepatocellular carcinoma (HCC) is among the most common and malignant cancers with no effective therapeutic approaches. Echinacoside (ECH), a phenylethanoid glycoside isolated from Chinese herbal medicine, Cistanche salsa, can inhibit HCC progression; however, poor absorption and low bioavailability limit its biological applications. METHODS: To improve ECH sensitivity to HepG2 cells, we developed a mesoporous silica nanoparticle (MSN)-based drug delivery system to deliver ECH to HepG2 cells via galactose (GAL) and poly(ethylene glycol) diglycidyl ether (PEGDE) conjugation (ECH@Au@MSN-PEGDE-GAL, or ECH@AMPG). Gain- and loss-of-function assays were conducted to assess the effects of UBR5 on HCC cell apoptosis and glycolysis. Moreover, the interactions among intermediate products were also investigated to elucidate the mechanisms by which UBR5 functions. RESULTS: The present study showed that ubiquitin protein ligase E3 component N-recognin 5 (UBR5) acted as an oncogene in HCC tissues and that its expression was inhibited by ECH. AMPG showed a high drug loading property and a slow and sustained release pattern over time. Moreover, owing to the valid drug accumulation, ECH@AMPG promoted apoptosis and inhibited glycolysis of HepG2 cells in vitro. In vivo experiments demonstrated that AMPG also enhanced the antitumor effects of ECH in HepG2 cell-bearing mice. CONCLUSIONS: Our results indicated the clinical significance of UBR5 as a therapeutic target. On the basis of the nontoxic and high drug-loading capabilities of AMPG, ECH@AMPG presented better effects on HCC cells compared with free ECH, indicating its potential for the chemotherapy of HCC.

[Retracted] MicroRNA­497 inhibits cellular proliferation, migration and invasion of papillary thyroid cancer by directly targeting AKT3.

Following the publication of this paper, it was drawn to the Editors' attention by a concerned reader that certain of the data shown for the cell migration and invasion assays in Figs. 2C and 5C were strikingly similar to data appearing in different form in other articles by different authors. Owing to the fact that the contentious data in the above article had already been published elsewhere, or were already under consideration for publication, prior to its submission to Molecular Medicine Reports, the Editor has decided that this paper should be retracted from the Journal. The authors were asked for an explanation to account for these concerns, but the Editorial Office did not receive a satisfactory reply. The Editor apologizes to the readership for any inconvenience caused. [Molecular Medicine Reports 16: 5815­5822, 2017; DOI: 10.3892/mmr.2017.7345].

microRNA-605 promotes cell proliferation, migration and invasion in non-small cell lung cancer by directly targeting LATS2.

[This retracts the article DOI: 10.3892/etm.2017.4538.].

MicroRNA-495 suppresses cell proliferation and invasion of hepatocellular carcinoma by directly targeting insulin-like growth factor receptor-1.

[This retracts the article DOI: 10.3892/etm.2017.5467.].

MicroRNA-139 targets fibronectin 1 to inhibit papillary thyroid carcinoma progression.

[This retracts the article DOI: 10.3892/ol.2017.7201.].

Therapeutic effects and the influence on serum inflammatory factors of high-flow nasal cannula oxygen therapy in senior patients with lower respiratory tract infections.

BACKGROUND: Lower respiratory tract infection (LRTI) is a clinical multi-infectious disease caused by viral, bacterial, and other microbial infections. OBJECTIVE: The present study aims to explore the therapeutic effects of high-flow nasal cannula (HFNC) oxygen therapy and its influence on the serum levels of inflammatory factors in senior patients with LRTI. METHODS: In this randomized controlled trial, 84 senior patients with LRTI were enrolled between March 2017 and December 2019 and divided into the observation group and the control group according to the random number table method, with 42 cases in each group. Conventional nasal cannula (CNC) oxygen therapy was conducted in the control group and HFNC was conducted in the observation group. After 3 days of treatment, sputum properties, sputum volume, sputum viscosity, and sputum crust formation were recorded to determine the clinical efficacy. ELISA was performed to detect the serum levels of tumor necrosis factor alpha (TNF-α) and interlukein (IL)-8 before and after treatment. RESULTS: The total efficacy in the observation group was 92.86%, which was higher than in the control group (73.81%) (P< 0.05). Three days after treatment, the percentage of grade I sputum in the observation group (73.81%) was higher than in the control group (40.48%). Moreover, the percentage of grade II sputum (23.81%), the percentage of grade III sputum (2.38%), together with the sputum crust formation rate in the observation group (4.76%) were all lower than in the control group (45.24, 14.28, and 26.19%, respectively) (P< 0.05). Three days after treatment, the levels of IL-8 (0.21 ± 0.03 pg/L) and TNF-α (1.27 ± 0.14 ng/L) in the observation group were lower than in the control group (0.30 ± 0.04 pg/L, and 1.49 ± 0.18 ng/L) (t= 6.525, 11.665, 6.252, respectively; P< 0.05). CONCLUSION: The application of HFNC in senior patients with LRTI could improve respiratory humidification, reduce the number of sputum aspirations, and improve anti-inflammatory effects. It is worthy of application in elderly patients with LRTI.

ß-Elemene induces apoptosis and autophagy in colorectal cancer cells through regulating the ROS/AMPK/mTOR pathway.

ß-Elemene is an effective anti-cancer ingredient extracted from the genus Curcuma (Zingiberaceae familiy). In the present study, we demonstrated that ß-elemene inhibited the proliferation of colorectal cancer cells and induced cell cycle arrest in the G2/M phase. In addition, ß-elemene induced nuclear chromatin condensation and cell membrane phosphatidylserine eversion, decreased cell mitochondrial membrane potential, and promoted the cleavage of caspase-3, caspase-9 and PARP proteins, indicating apoptosis in colorectal cancer cells. At the same time, ß-elemene induced autophagy response, and the treated cells showed autophagic vesicle bilayer membrane structure, which was accompanied by up-regulation of the expression of LC3B and SQSTM1. Furthermore, ß-elemene increased ROS levels in colorectal cancer cells, promoted phosphorylation of AMPK protein, and inhibited mTOR protein phosphorylation. In the experiments in vivo, ß-elemene inhibited the tumor size and induced apoptosis and autophagy in nude mice. In summary, ß-elemene inhibited the occurrence and development of colon cancer xenografts in nude mice, and significantly induced apoptosis and autophagy in colorectal cancer cells in vitro. These effects were associated with regulation of the ROS/AMPK/mTOR signaling. We offered a molecular basis for the development of ß-elemene as a promising anti-tumor drug candidate for colorectal cancer.