A Randomized, Double-Blind, Controlled Clinical Study on the Curative Effect of Huaier on Mild-to-Moderate Psoriasis and an Experimental Study on the Proliferation of Hacat Cells

The antitumor effects of Huaier have been recently revealed. However, no research has been conducted on the effects of Huaier on keratinocyte proliferation and for the treatment of psoriasis. Hacat cells were treated with different concentrations of Huaier for different periods of times. The effects on cell proliferation and vitality and on the cell cycle were detected. Patients with mild-to-moderate psoriasis were randomized and divided into two groups in a double-blind manner. The experimental group was given sugar-free Yinxie granules and Huaiqihuang (HQH) granules, and the control group was given sugar-free Yinxie granules and placebo. After 4 weeks, various therapeutic indexes were compared. Huaier significantly inhibited Hacat cell proliferation, suppressed vitality, and blocked the cell cycle in the G1 phase compared with the control group (P < 0.01, respectively). After treatment for 4 weeks, the number of patients between the two groups that experienced a 50% reduction in the Psoriasis Area and Severity Index (PASI 50), PASI 75 and PASI 90, was significantly different (P <0.01). The body surface area (BSA) affected by psoriasis and static physician’s global assessment (sPGA) was significantly reduced (P < 0.01); additionally, a significant improvement in the Dermatology Life Quality Index (DLQI) (P < 0.01) was observed. Huaier has shown promising effects in both clinical and experimental setting in this preliminary study and it might provide some benefit in the treatment of psoriasis vulgaris in the future.

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TRB3 is elevated in psoriasis vulgaris lesions and mediates HaCaT cells proliferation in vitro

Journal of Investigative Medicine ◽

10.1136/jim-2017-000453 ◽

2017 ◽

Vol 65 (7) ◽

pp. 1084-1088 ◽

Cited By ~ 3

Author(s):

Xiao-Jing Yu ◽

Tie-Jun Song ◽

Lu-Wei Zhang ◽

Ying Su ◽

Ke-Yu Wang ◽

...

Keyword(s):

Cell Cycle ◽

Cell Proliferation ◽

Messenger Rna ◽

Psoriasis Vulgaris ◽

Metabolic Diseases ◽

Brdu Incorporation ◽

Cell Cycle Distribution ◽

Hacat Cells ◽

Keratinocyte Proliferation

Psoriasis is a chronic skin disease characterized by abnormal keratinocyte proliferation and differentiation, inflammation, and angiogenesis. Overexpression of tribbles homolog3 (TRB3), which belongs to the tribbles family of pseudokinases, has been found in several human tumors and metabolic diseases, but its role in psoriasis has not been fully clarified. The aim of this study is to investigate the expression of TRB3 in psoriasis and explore its roles in the proliferation of keratinocytes. Twenty-four patients with psoriasis vulgaris were recruited for the study. Diagnosis of psoriasis was based on clinical and histologic examinations. Immunohistochemistry and real-time reverse transcription PCR (RT-PCR) were performed to determine protein and messenger RNA (mRNA) expression of TRB3 in psoriasis lesions. 5-Bromo-2-deoxyUridine (BrdU) incorporation assay were performed for cell proliferation. Cell cycle distribution was assessed by flow cytometry analysis. The levels of TRB3 is elevated in psoriatic lesions compared with psoriatic non-lesions. The HaCat cells expressed the TRB3 gene. We found TRB3 silencing to significantly inhibit HaCat cell proliferation. Furthermore, the specific knockdown of TRB3 slowed down the cell cycle at the gap 0/first gap phase. In conclusion, our data suggest that TRB3 is overexpressed in lesions of patients with psoriasis and may be involved in the abnormal proliferation of keratinocytes. Therefore, TRB3 may be a potential therapeutic target for psoriasis.

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Modulation effects of hexamethylene bisacetamide on growth and differentiation of cultured human malignant glioma cells

Journal of Neurosurgery ◽

10.3171/jns.1996.84.5.0831 ◽

1996 ◽

Vol 84 (5) ◽

pp. 831-838 ◽

Cited By ~ 13

Author(s):

Xiao-Nan Li ◽

Zi-Wei Du ◽

Qiang Huang

Keyword(s):

Cell Cycle ◽

Cell Proliferation ◽

Malignant Glioma ◽

Culture Media ◽

Morphological Changes ◽

Control Group ◽

Cell Cycle Distribution ◽

Content Type ◽

Hexamethylene Bisacetamide ◽

Human Malignant Glioma

✓ The modulation effects of hexamethylene bisacetamide (HMBA), a differentiation-inducing agent, on growth and differentiation of cells from human malignant glioma cell line SHG-44 were studied. At cytostatic doses (2.5 mM, 5 mM, 7.5 mM, and 10 mM for 15 days), HMBA exerted a marked inhibitory effect on cell proliferation. Exposure to HMBA (5 mM and 10 mM for 12 days) also resulted in an accumulation of cells in G0/G1 phase and a decrease of cells in S phase as analyzed by flow cytometry. The reversible effects of 7.5 mM HMBA and 10 mM HMBA on cell proliferation and 10 mM HMBA on disruption of cell cycle distribution were observed when HMBA was removed from culture media on Day 6 and replaced with HMBA-free media. Colony-forming efficiency (CFE) in soft agar was remarkably decreased by HMBA (2.5 mM, 5 mM, 7.5 mM, and 10 mM for 14 days), and in 7.5 mM HMBA— and 10 mM HMBA—treated cells, the CFEs were reduced to 25% and 12.5%, respectively, of that in untreated cells. Cells treated with HMBA (5 mM and 10 mM for 15 days) remained tumorigenic in athymic nude mice, but the growth rates of the xenografts were much slower than those in the control group. The effects of HMBA on cell proliferation, cell cycle distribution, CFE, and growth of xenografts were dose dependent. A more mature phenotype was confirmed by the morphological changes from spindle shape to large polygonal stellate shape and remarkably elevated expression of glial fibrillary acidic protein in cells exposed to HMBA (5 mM, 10 mM for 15 days). Our results showed that a more differentiated phenotype with marked growth arrest was induced in SHG-44 cells by HMBA.

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A randomised, open label comparative study of hydroxychloroquine with betamethasone oral mini pulse in the management of patients with alopecia areata

International Journal of Basic & Clinical Pharmacology ◽

10.18203/2319-2003.ijbcp20210189 ◽

2021 ◽

Vol 10 (2) ◽

pp. 187

Author(s):

Jeyasudha Jambusayee ◽

Kulur Mukhyaprana Sudha

Keyword(s):

Alopecia Areata ◽

Life Quality ◽

Autoimmune Disorder ◽

Study Groups ◽

Pulse Therapy ◽

The Body ◽

Control Group ◽

Study Group ◽

Open Label ◽

Significant Difference

Background: Alopecia areata is an autoimmune disorder causing patchy hair loss on scalp and other parts of the body and leading to poor self-esteem and anxiety in patients. Treatment with topical or systemic drugs like steroids or other immunosuppressants is associated with adverse effects. Hydroxychloroquine is an antimalarial drug, with T cell modulating function. This study was undertaken to assess the safety, efficacy and tolerability of Hydroxychloroquine in Alopecia areata compared to betamethasone oral mini pulse (OMP) therapy. Methods: 60 patients with alopecia areata were randomized into two groups of 30 each. Control group received tab. betamethasone 5 mg/day on two consecutive days of week for 12 weeks and Study group received tab. hydroxychloroquine 200 mg/day for 12 weeks. They were followed-up for further 12 weeks. Scale of alopecia tool, dermatology life quality index and global assessment at baseline, 12 weeks and 24 weeks were used to assess the outcome.Results: 94 patients were screened and 60 patients were included. All patients completed the study. At the end of 12 weeks, there was a statistically significant reduction in SALT and DLQI scores in both control and study groups. But at the end of 24 weeks, the study group showed an increase in the scores. Relapses were more in the study group. No significant difference in the incidence of adverse events was noted between the two groups.Conclusions: Hydroxychloroquine 200 mg/day is less efficacious in the management of alopecia areata in comparison to betamethasone oral mini pulse therapy.

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Lysophosphatidic Acid Mediates Imiquimod-Induced Psoriasis-like Symptoms by Promoting Keratinocyte Proliferation through LPAR1/ROCK2/PI3K/AKT Signaling Pathway

International Journal of Molecular Sciences ◽

10.3390/ijms221910777 ◽

2021 ◽

Vol 22 (19) ◽

pp. 10777

Author(s):

Donghee Kim ◽

Hyo-Jin Kim ◽

Jin-Ok Baek ◽

Joo-Young Roh ◽

Hee-Sook Jun

Keyword(s):

Cell Cycle ◽

Lysophosphatidic Acid ◽

Cell Cycle Progression ◽

Akt Signaling ◽

Inflammasome Activation ◽

Hacat Cells ◽

Cycle Progression ◽

Keratinocyte Proliferation ◽

P27kip1 Expression ◽

Cyclin A2

Psoriasis is a chronic inflammatory skin disease. Recently, lysophosphatidic acid (LPA)/LPAR5 signaling has been reported to be involved in both NLRP3 inflammasome activation in macrophages and keratinocyte activation to produce inflammatory cytokines, contributing to psoriasis pathogenesis. However, the effect and molecular mechanisms of LPA/LPAR signaling in keratinocyte proliferation in psoriasis remain unclear. In this study, we investigated the effects of LPAR1/3 inhibition on imiquimod (IMQ)-induced psoriasis-like mice. Treatment with the LPAR1/3 antagonist, ki16425, alleviated skin symptoms in IMQ-induced psoriasis-like mouse models and decreased keratinocyte proliferation in the lesion. It also decreased LPA-induced cell proliferation and cell cycle progression via increased cyclin A2, cyclin D1, cyclin-dependent kinase (CDK)2, and CDK4 expression and decreased p27Kip1 expression in HaCaT cells. LPAR1 knockdown in HaCaT cells reduced LPA-induced proliferation, suppressed cyclin A2 and CDK2 expression, and restored p27Kip1 expression. LPA increased Rho-associated protein kinase 2 (ROCK2) expression and PI3K/AKT activation; moreover, the pharmacological inhibition of ROCK2 and PI3K/AKT signaling suppressed LPA-induced cell cycle progression. In conclusion, we demonstrated that LPAR1/3 antagonist alleviates IMQ-induced psoriasis-like symptoms in mice, and in particular, LPAR1 signaling is involved in cell cycle progression via ROCK2/PI3K/AKT pathways in keratinocytes.

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191 RISK ASSESSMENT OF BISPHENOL A, AN ENDOCRINE DISRUPTOR, VIA PROLIFERATIVE EFFECT ON THE GROWTH OF ESTROGEN-DEPENDENT OVARIAN CANCER IN CELLULAR AND ANIMAL MODELS

Reproduction Fertility and Development ◽

10.1071/rdv25n1ab191 ◽

2013 ◽

Vol 25 (1) ◽

pp. 244

Author(s):

K.-A. Hwang ◽

K.-C. Choi

Keyword(s):

Cell Cycle ◽

Ovarian Cancer ◽

Cell Proliferation ◽

Bisphenol A ◽

Cancer Cells ◽

The Body ◽

Brdu Incorporation ◽

Ovarian Cancer Cells ◽

Tumour Proliferation

One of estrogens in the body, 17β-oestradiol (E2), is a pleiotropic hormone that regulates the growth and differentiation of many tissues and also acts as a mitogen that promotes the development and proliferation of hormone-responsive cancers such as breast and ovarian carcinomas. Xenoestrogens are chemical compounds that imitate oestrogen in living organisms and are classified as a type of endocrine-disrupting chemical (EDC). Bisphenol A (BPA) is a widely used industrial compound, and also known as an EDC and especially a xenoestrogen. In this study, we examined the effect of E2 or BPA on the cell growth of BG-1 ovarian cancer cells in vivo and in vitro. In the cell proliferation assay in vitro, E2 or BPA increased the growth of the BG-1 ovarian cancer cells expressing oestrogen receptors (ER). Their proliferation activity was reversed by the treatment of ICI 182 780, a well-known antagonist of ER, which demonstrates that the cell proliferation by E2 or BPA is mediated by ER and BPA certainly acts as a xenoestrogen in the BG-1 ovarian cancer cells. Clearly, E2 and BPA increased the expression of cyclin D1, a factor responsible for the G1/S cell cycle transition. These reagents also decreased the expression of p21, a potent cyclin-dependent kinase (CDK) inhibitor that arrests the cell cycle in the G1 phase. As a result, they promoted the proliferation of BG-1 cells via upregulation of the cell cycle progression. In mice xenograft models transplanted with BG-1 ovarian cancer cells, E2 or BPA administration significantly induced the tumour proliferation compared with vehicle (corn oil) treatment for 10 weeks, which was identified by the measurement of tumour volume and histological analysis on tumour tissues such as hematoxylin and eosin (H&E) staining and BrdU incorporation assay. Taken together, as an EDC having a xenoestrogenic activity, BPA was demonstrated to have a risk of tumour proliferation in oestrogen-dependent cancers such as ovarian cancer. This work was supported by a National Research Foundation of Korea (NRF) grant funded by the Ministry of Education, Science and Technology (MEST) of government of Korea (no. 2011-0015385).

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SUZ12 Participates in PNH Cloning Proliferation By Regulating Histone H3K27me3 Methylation Level

Blood ◽

10.1182/blood-2021-148546 ◽

2021 ◽

Vol 138 (Supplement 1) ◽

pp. 1106-1106

Author(s):

Rong Fu ◽

Yingying Chen ◽

Zonghong Shao ◽

Hui Liu ◽

Lijie Zeng ◽

...

Keyword(s):

Cell Cycle ◽

Cell Proliferation ◽

Protein Expression ◽

Peripheral Blood ◽

Methylation Level ◽

Cell Model ◽

Gene Mutations ◽

Control Group ◽

Mrna And Protein Expression ◽

And Control

Abstract Paroxysmal nocturnal hemoglobinuria (PNH) is a disease of hematopoietic stem cell membrane defects due to acquired PIG-Amutation. Our previous study found some secondary gene mutations in PNH patients by WES. However, it is not clear exactly which mutations are associated with the disease. So, 97 target genes were selected as a target gene panel and tested in 23 PNH patients by DNA sequencing of specific target regions. We found that all PNH patients had other gene mutations except PIG-Amutations, including TTN, NCOR2, CPS1, MUC4, SUZ12, LFNG, CELSR2, JAK2, SETBP1 and KMT2D (Figure1A). Through harmful analysis, KEGG enrichment, GO enrichment analysis and protein interaction analysis, we screened out the secondary mutant gene SUZ12 that may be involved in the cloning proliferation of PNH. We detected the mRNA and protein expression levels of SUZ12 and H3K27me3 methylation in PNH patients and health volunteers, the results showed that the mRNA and protein expression levels of SUZ12 and H3K27me3 methylation in peripheral blood CD59 -cells of PNH patients were higher than those in CD59 + cells of PNH patients and healthy controls (Figure1B). The relative expression level of SUZ12 in peripheral blood CD59 -cells of PNH patients was correlated with (r=0.4162, p=0.0385), CD59 -erythrocyte ratio (r=0.4636, p=0.0196), CD59 -monocyte ratio (r=0.4052, p=0.0495), Flaer -monocyte ratio (r=0.6769, p=0.0004) and Flaer -granulocytic ratio (r=0.6146, p=0.0018), indicating that SUZ12 may be involved in abnormal PNH cloning and proliferation by regulating H3K27me3. To verify the role of SUZ12 in the proliferation of PNH cloning, we used CRISPR/Cas9 to knockdown PIG-A expression in THP-1 cells to construct A PNH cell model, the expression level of PIG-A protein in the cell model was significantly decreased, and the proportion of CD59 - cells accounted was stable at 95%. Then lentivirus transfection was used to knockdown the expression of SUZ12 in PNH cell model. The results showed when the SUZ12 expression was knockdown, the methylation level of histone H3K27me3 was decreased, the cell proliferation activity was decreased, apoptosis was increased, and the cell cycle was arrested at G0/G1 phase. The proportion of CD59 + cells increased gradually from 3 weeks after transfection, and significantly increased at 4 weeks after transfection, while no changes were observed in the empty virus group and control group (Figure1C). Four weeks after lentivirus transfection, the expression of PIG-A protein recovered in SUZ12 knockdown group compared with empty virus group and control group (Figure1D). In conclusion, SUZ12 mutation leads to the overexpression of SUZ12, which can affect cell proliferation, apoptosis and cell cycle by regulating the methylation level of histone H3K27me3, thereby promoting the proliferation of PNH abnormal cloning and participating in the pathogenesis of PNH. Figure 1 Figure 1. Disclosures No relevant conflicts of interest to declare.

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Internalization of Titanium Dioxide Nanoparticles Is Cytotoxic for H9c2 Rat Cardiomyoblasts

Molecules ◽

10.3390/molecules23081955 ◽

2018 ◽

Vol 23 (8) ◽

pp. 1955 ◽

Cited By ~ 13

Author(s):

Elizabeth Huerta-García ◽

Iván Zepeda-Quiroz ◽

Helen Sánchez-Barrera ◽

Zaira Colín-Val ◽

Ernesto Alfaro-Moreno ◽

...

Keyword(s):

Oxidative Stress ◽

Cell Cycle ◽

Cell Proliferation ◽

Cell Death ◽

Titanium Dioxide ◽

Titanium Dioxide Nanoparticles ◽

Membrane Integrity ◽

The Body ◽

Potential Health ◽

Tio2 Nps

Titanium dioxide nanoparticles (TiO2 NPs) are widely used in industry and daily life. TiO2 NPs can penetrate into the body, translocate from the lungs into the circulation and come into contact with cardiac cells. In this work, we evaluated the toxicity of TiO2 NPs on H9c2 rat cardiomyoblasts. Internalization of TiO2 NPs and their effect on cell proliferation, viability, oxidative stress and cell death were assessed, as well as cell cycle alterations. Cellular uptake of TiO2 NPs reduced metabolic activity and cell proliferation and increased oxidative stress by 19-fold measured as H2DCFDA oxidation. TiO2 NPs disrupted the plasmatic membrane integrity and decreased the mitochondrial membrane potential. These cytotoxic effects were related with changes in the distribution of cell cycle phases resulting in necrotic death and autophagy. These findings suggest that TiO2 NPs exposure represents a potential health risk, particularly in the development of cardiovascular diseases via oxidative stress and cell death.

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Curcumin Reverses NNMT-Induced 5-Fluorouracil Resistance via Increasing ROS and Cell Cycle Arrest in Colorectal Cancer Cells

Biomolecules ◽

10.3390/biom11091295 ◽

2021 ◽

Vol 11 (9) ◽

pp. 1295

Author(s):

Guoli Li ◽

Sining Fang ◽

Xiao Shao ◽

Yejia Li ◽

Qingchao Tong ◽

...

Keyword(s):

Colorectal Cancer ◽

Cell Cycle ◽

Cell Proliferation ◽

Cell Cycle Arrest ◽

Cell Lines ◽

Induced Resistance ◽

Phase Cell ◽

Ros Generation ◽

Antitumor Effects ◽

Cycle Arrest

Nicotinamide N-methyltransferase (NNMT) plays multiple roles in improving the aggressiveness of colorectal cancer (CRC) and enhancing resistance to 5-Fluorouracil (5-FU), making it an attractive therapeutic target. Curcumin (Cur) is a promising natural compound, exhibiting multiple antitumor effects and potentiating the effect of 5-FU. The aim of the present study is to explore the effect of Cur on attenuating NNMT-induced resistance to 5-FU in CRC. A panel of CRC cell lines with different NNMT expressions are used to characterize the effect of Cur. Herein, it is observed that Cur can depress the expression of NNMT and p-STAT3 in CRC cells. Furthermore, Cur can induce inhibition of cell proliferation, G2/M phase cell cycle arrest, and reactive oxygen species (ROS) generation, especially in high-NNMT-expression CRC cell lines. Cur can also re-sensitize high-NNMT-expression CRC cells to 5-FU both in vitro and in vivo. In summary, it is proposed that Cur can reverse NNMT-induced cell proliferation and 5-FU resistance through ROS generation and cell cycle arrest. Given that Cur has long been used, we suppose that Cur is a promising anticancer drug candidate with minimal side effects for human CRC therapy and can attenuate NNMT-induced resistance to 5-FU.

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Inhibitory effect and mechanism of action (MOA) of hirsutine on the proliferation of T-cell leukemia Jurkat clone E6-1 cells

PeerJ ◽

10.7717/peerj.10692 ◽

2021 ◽

Vol 9 ◽

pp. e10692

Author(s):

Jie Meng ◽

Rui Su ◽

Luping Wang ◽

Bo Yuan ◽

Ling Li

Keyword(s):

Cell Cycle ◽

Flow Cytometry ◽

Cell Proliferation ◽

Cell Death ◽

T Cell ◽

Mechanism Of Action ◽

Mrna Levels ◽

T Cell Leukemia ◽

Cell Leukemia ◽

Antitumor Effects

Background The bark of Uncaria rhynchophylla has been traditionally used to treat convulsion, bleeding, hypertension, auto-immune conditions, cancer, and other diseases. The main focus of this research is done for the purpose of exploring the antitumor activity and mechanism of action (MOA) for hirsutine isolated from U. rhynchophylla. Methods Jurkat clone E6-1 cells were treated using 10, 25 and 50 μM for 48 h. Inhibition of cell proliferation due to hirsutine treatment was evaluated by CCK8 assay. Flow cytometry was applied to ascertain Jurkat cell cycle progression and apoptosis after treatment with 10, 25 and 50 μM hirsutine for 48 h. The expression and level of the apoptosis-related genes and proteins was analyzed by Real-time Quantitative polymerase chain reaction (qPCR) and Western blotting method, respectively. Results CCK8 analyses revealed that hirsutine could significantly inhibit the proliferation of Jurkat clone E6-1 cells, in a concentration and time-dependent fashion. Flow cytometry assays revealed that hirsutine could drive apoptotic death and G0/G1 phase arrest in Jurkat cells. Apoptotic cells frequencies were 4.99 ± 0.51%, 13.69 ± 2.00% and 40.21 ± 15.19%, and respective cell cycle arrest in G0/G1 accounted for 34.85 ± 1.81%, 42.83 ± 0.70% and 49.12 ± 4.07%. Simultaneously, compared with the control group, Western blot assays indicated that the up-regulation of pro-apoptotic Bax, cleaved-caspase3, cleaved-caspase9 and Cyto c proteins, as well as the down-regulation of Bcl-2 protein which guards against cell death, might be correlated with cell death induction and inhibition of cell proliferation. QPCR analyses indicated that hirsutine could diminish BCL2 expression and, at the same time, improve Bax, caspase-3 and caspase-9 mRNA levels, thus reiterating a putative correlation of hirsutine treatment in vitro with apoptosis induction and inhibition of cell proliferation (p-value < 0.05). Excessive hirsutine damages the ultrastructure in mitochondria, leading to the release of Cyt c from the mitochondria to cytoplasm in Jurkat clone E6-1 cells, thereby inducing the activated caspase cascade apoptosis process through a mitochondria-mediated pathway. Conclusion An important bioactive constituent—hirsutine—appears to have antitumor effects in human T-cell leukemia, thus enlightening the use of phytomedicines as a novel source for tumor therapy. It is speculated that hirsutine may induce apoptosis of Jurkat Clone E6-1 cells through the mitochondrial apoptotic pathway.

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Lenvatinib Promotes the Antitumor Effects of Doxorubicin in Anaplastic Thyroid Cancer

10.21203/rs.3.rs-29005/v1 ◽

2020 ◽

Author(s):

Xi Su ◽

Jiaxin Liu ◽

Haihong Zhang ◽

Qingqing Gu ◽

Xinrui Zhou ◽

...

Keyword(s):

Cell Cycle ◽

Cell Proliferation ◽

Thyroid Cancer ◽

Combination Therapy ◽

Cell Cycle Arrest ◽

Anaplastic Thyroid Cancer ◽

Antitumor Efficacy ◽

Potential Candidate ◽

Antitumor Effects ◽

Cycle Arrest

Abstract Background Anaplastic thyroid cancer (ATC) is a kind of rare thyroid cancer with very poor prognosis. It is one of the deadliest cancers in human due to the aggressive behavior and resistance to treatment. Doxorubicin has been approved in ATC treatment as a single agent, but monotherapy still shows no improvement of the total survival in advanced ATC. Lenvatinib was investigated with encouraging results in treating the patients with radioiodine-refractory differentiated thyroid cancer (DTC). However, antitumor efficacy of combination therapy with lenvatinib and doxorubicin remains largely unclear. Methods The antitumor efficacy of combination therapy with lenvatinib and doxorubicin on ATC cell proliferation and was assessed by the MTT assay and colony formation. Flow cytometry were employed to assess ATC cells’ apoptosis and cell cycle arrest in response to combination therapy. Xenograft models were used to test its in vivo antitumor activity. Result Lenvatinib monotherapy was less effective than doxorubicin in treating ATC cell lines and xenografts model. The combination therapy of lenvatinib and doxorubicin significantly inhibited ATC cell proliferation and tumor growth in nude mice, and induced cell apoptosis and cell cycle arrest in compared to lenvatinib or doxorubicin monotherapy. Conclusion Lenvatinib promotes the antitumor effects of doxorubicin in ATC cell and xenografts model. Lenvatinib/doxorubicin combination may be a potential candidate therapeutic approach for ATC.

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