Journal: Discover Oncology

Article Title: Anlotinib inhibits esophageal cancer malignancy by ameliorating the immune microenvironment

doi: 10.1007/s12672-026-04457-8

Figure Lengend Snippet: Anlotinib inhibited the proliferation of EC cells both in vitro andin vivo. A , B Anlotinib sensitivity assay showsthat the value of IC50 of ECA109 cells is 2992 nM and the value of IC50 of KYSE150 cells is 2279 nM. C , D Cell survivalassay shows that anlotinib can inhibit the growth of ECA109 cells and KYSE150 cells treated with 2.5μmol anlotinib. E Representative xenografted tumors from Anlotinib group and the control group. F The curves of tumor volumesof mice in the Anlotinib group and the control group as indicted time. G The tumor weight in the Anlotinib groupis significantly smaller than that in the control group. H The curves of body weights of mice in the Anlotinib groupand the control group as indicted time time. The t test was used for statistic quantifications: *p < 0.05, ***p < 0.001,****p < 0.0001

Article Snippet: Anlotinib (AL3818) dihydrochloride was purchased from Selleck, and its stock solution was prepared according to the manufacturer’s instructions.

Techniques: In Vitro, Sensitive Assay, Control

Journal: Discover Oncology

Article Title: Anlotinib inhibits esophageal cancer malignancy by ameliorating the immune microenvironment

doi: 10.1007/s12672-026-04457-8

Figure Lengend Snippet: Anlotinib regulated immune infiltration through VEGFR2. A The mRNA level of VEGFR2 was examined by quantitative PCR. B The expression of marker genes related to immune cells was examined by quantitative PCR. C Analysis of public databases shows that the high expression of VEGFR2 is significantly associated with a high overall survival rate in anti-PD-1, PD-L1 and CTLA-4 immunotherapies. D Analysis of public databases shows that the high expression of VEGFR2 is significantly associated with a high disease-free survival rate in anti-PD-1, PD-L1 and CTLA-4 immunotherapies. The t test was used for statistic quantifications: *** p < 0.001, ns, not significant.

Article Snippet: Anlotinib (AL3818) dihydrochloride was purchased from Selleck, and its stock solution was prepared according to the manufacturer’s instructions.

Techniques: Real-time Polymerase Chain Reaction, Expressing, Marker

Journal: Frontiers in Oncology

Article Title: Case Report: Anlotinib Therapy in a Patient With Recurrent and Metastatic RAIR-DTC Harboring Coexistent TERT Promoter and BRAF V600E Mutations

doi: 10.3389/fonc.2021.626076

Figure Lengend Snippet: Treatment prior to anlotinib therapy. (A) Timeline of treatment prior to clinical study, including four operations in the neck, two sessions of RAI therapy and TSH suppression therapy with L-T4. (B) Functional iodine uptake was observed in the neck on the initial post-treatment whole-body scan. (C) No functional iodine uptake was observed in the neck on the second post-therapy whole-body scan, but an abnormal radioactive iodine uptake foci in anterior-inferior mediastinum. (D) Abnormal radioactive iodine uptake foci in anterior-inferior mediastinum was confirmed to be external contamination by change clothes. (E) Papillary thyroid carcinoma was confirmed pathologically with specimen from the 4th operation (HE stain, x200) after RAIR-DTC was developed, and Ki67 stain revealed about 10% positive rate. Tg, Thyroglobulin; TSH, Thyroid Stimulating Hormone; L-CND, Left-Central Neck Dissection; L-LND, Left-Lateral Neck Dissection; RAI, Radioactive Iodine.

Article Snippet: Anlotinib is a multitarget tyrosine kinase inhibitor that was originally designed to inhibit VEGFR2/3, FGFR1-4, PDGFRα/β, c-Kit, and Ret , thereby exerting inhibitory effects on tumor angiogenesis and growth , tumor invasion , lymphangiogenesis and lymphatic metastasis ( ).

Techniques: Functional Assay, H&E Stain, Staining, Dissection

Journal: Frontiers in Oncology

Article Title: Case Report: Anlotinib Therapy in a Patient With Recurrent and Metastatic RAIR-DTC Harboring Coexistent TERT Promoter and BRAF V600E Mutations

doi: 10.3389/fonc.2021.626076

Figure Lengend Snippet: Tumor shrinkage during placebo and anlotinib therapy. (A) Imaging evaluation on target and non-target lesions, including placebo therapy (baseline, C2, C8) and anlotinib therapy (baseline, C2, C8, C16, and C52). (①: Tumor under the right subclavian; ②: Tumor in front of the right sternocleidomastoid muscle; ③: Tumor behind the left scapula; ④: Tumor in front of larynx and tumor in the cervical sheath; ⑤: Metastatic tumor of the left lung). Red Arrow: tumor. (B) Tumor shrinkage per review (Evaluation was performed before C12 in every two cycles and after C12 in every four cycles).

Article Snippet: Anlotinib is a multitarget tyrosine kinase inhibitor that was originally designed to inhibit VEGFR2/3, FGFR1-4, PDGFRα/β, c-Kit, and Ret , thereby exerting inhibitory effects on tumor angiogenesis and growth , tumor invasion , lymphangiogenesis and lymphatic metastasis ( ).

Techniques: Imaging

Journal: Frontiers in Oncology

Article Title: Case Report: Anlotinib Therapy in a Patient With Recurrent and Metastatic RAIR-DTC Harboring Coexistent TERT Promoter and BRAF V600E Mutations

doi: 10.3389/fonc.2021.626076

Figure Lengend Snippet: TSH suppression therapy during anlotinib treatment. (A) Change of serum TT4 and FT4 during placebo and anlotinib therapy (Yellow dotted line: upper limit of FT4, Normal range: 12–22 pmol/L; Red dotted line: upper limit of TT4, Normal range: 66–181 nmol/L). (B) Change of serum TSH and Tg during placebo and anlotinib therapy (TSH normal range: 0.27–4.2 μIU/mL; Tg normal range: 3.5–77 ng/mL).

Article Snippet: Anlotinib is a multitarget tyrosine kinase inhibitor that was originally designed to inhibit VEGFR2/3, FGFR1-4, PDGFRα/β, c-Kit, and Ret , thereby exerting inhibitory effects on tumor angiogenesis and growth , tumor invasion , lymphangiogenesis and lymphatic metastasis ( ).

Techniques:

Journal: Frontiers in Oncology

Article Title: Targeting liposarcoma: unveiling molecular pathways and therapeutic opportunities

doi: 10.3389/fonc.2024.1484027

Figure Lengend Snippet: Clinical trials related to LPS-targeted therapy.

Article Snippet: ALTER-0202 (NCT01878448) , Anlotinib , A multikinase angiogenesis inhibitor , II , 166 STS pts , LPS (n = 13) , PFR12 weeks , – , LPS PFR 12weeks:63% LPS mPFS:5.6m LPS mOS:13 m LPS ORR:7.7% , Yihebali Chi , 2018 , ( ) .

Techniques: Clinical Proteomics, Activity Assay

Journal: Frontiers in Oncology

Article Title: Targeting liposarcoma: unveiling molecular pathways and therapeutic opportunities

doi: 10.3389/fonc.2024.1484027

Figure Lengend Snippet: Clinical trials of LPS-targeted and immunotherapy are currently underway.

Article Snippet: ALTER-0202 (NCT01878448) , Anlotinib , A multikinase angiogenesis inhibitor , II , 166 STS pts , LPS (n = 13) , PFR12 weeks , – , LPS PFR 12weeks:63% LPS mPFS:5.6m LPS mOS:13 m LPS ORR:7.7% , Yihebali Chi , 2018 , ( ) .

Techniques: Clinical Proteomics, Bioprocessing, Blocking Assay, Expressing, Activity Assay

Journal: Cell Death & Disease

Article Title: Directly targeting c-Myc contributes to the anti-multiple myeloma effect of anlotinib

doi: 10.1038/s41419-021-03685-w

Figure Lengend Snippet: A Chemical structure of anlotinib. B MM cell lines (NCI-H929, RPMI-8226, LP1, MM.1S, OPM2, and U266) were treated with anlotinib (0–20 μM) for 48 h, and the cell viability was detected by CCK8. The IC50 value was calculated based on the dose–response curve using Prism 8.0 software. C – E NCI-H929, RPMI-8226 and LP1 cells were treated with anlotinib for 24 and 48 h, followed by the assessment of cell viability. F The CD138 + and G CD138 − cells isolated from MM patients were treated with anlotinib (0–10 μM) for 24 h, and then the cell viability was assessed. H Normal BMMCs from four healthy donors were treated with anlotinib (0–10 μM) for 24 h. Data are shown as mean ± SD and representative of three independent experiments.

Article Snippet: Anlotinib, CHX and MG-132 were purchased from CSNpharm (Chicago, IL, USA), dissolved in Dimethyl Sulfoxide (Sigma, St. Louis, MO) and stored in dark at −20 °C until use.

Techniques: Software, Isolation

Journal: Cell Death & Disease

Article Title: Directly targeting c-Myc contributes to the anti-multiple myeloma effect of anlotinib

doi: 10.1038/s41419-021-03685-w

Figure Lengend Snippet: A , B NCI-H929 and RPMI-8226 cells were co-cultured with or without BMSCs, and then treated with anlotinib (0–10 μM) for 48 h. After staining with Annexin V and PI, flow cytometry analysis was performed to assess the apoptosis rate. C , D NCI-H929 and RPMI-8226 cells were treated with anlotinib (0–10 μM) for 48 h, in the presence or absence of IL-6 (10 ng/ml). Cell proliferation was measured by CCK-8 assay. ** P < 0.01; *** P < 0.001; NS P > 0.05. Data are shown as mean ±SD and from three independent experiments.

Article Snippet: Anlotinib, CHX and MG-132 were purchased from CSNpharm (Chicago, IL, USA), dissolved in Dimethyl Sulfoxide (Sigma, St. Louis, MO) and stored in dark at −20 °C until use.

Techniques: Cell Culture, Staining, Flow Cytometry, CCK-8 Assay

Journal: Cell Death & Disease

Article Title: Directly targeting c-Myc contributes to the anti-multiple myeloma effect of anlotinib

doi: 10.1038/s41419-021-03685-w

Figure Lengend Snippet: A NCI-H929 and RPMI-8226 cells were treated with 5 µM anlotinib for the indicated time. Cell cycle was analyzed by flow cytometry. The numerical percentage shown indicates the G 2 /M population. B The morphology of NCI-H929 and RPMI-8226 cells after anlotinib treatment (5 μM, 24 h) was observed by Wright staining. Scale bar: 20 μm. C Representative images of TUNEL and DAPI staining for cells treated with anlotinib (5 μM, 24 h). The green dot represents positive TUNEL staining. The blowup images from the red boxes showed a significant fraction of nuclei after anlotinib exposure. Scale bar: 20 μm. D NCI-H929 and RPMI-8226 cells were treated with anlotinib (0–10 μM) for 24 h. Whole cell lysates were subjected to western blotting using antibodies against PARP-1, caspase 3, caspase 9, and β-actin. E Cells were treated as described in D , and apoptosis was detected by flow cytometry using Annexin V/PI staining. The percentages of apoptotic cells were shown in the histogram from three independent experiments. Each experiment was performed in triplicate. Con: control group; Anlo: anlotinib group. *** P < 0.001.

Article Snippet: Anlotinib, CHX and MG-132 were purchased from CSNpharm (Chicago, IL, USA), dissolved in Dimethyl Sulfoxide (Sigma, St. Louis, MO) and stored in dark at −20 °C until use.

Techniques: Flow Cytometry, Wright Stain, TUNEL Assay, Staining, Western Blot, Control

Journal: Cell Death & Disease

Article Title: Directly targeting c-Myc contributes to the anti-multiple myeloma effect of anlotinib

doi: 10.1038/s41419-021-03685-w

Figure Lengend Snippet: A Volcano plot of the DEGs from the transcriptomes of the control and anlotinib group ( P < 0.05, Fold change > 1.5). B KEGG analysis of the DEGs. C NCI-H929 and RPMI-8226 cells were treated with anlotinib (5 μM) for the indicated time. Whole cell lysates were subjected to western blotting. D Heatmaps of the top 40 downregulated c-Myc target genes in NCI-H929 cells treated with anlotinib versus DMSO for 12 h. Rows show Z -scores are calculated for each cell type. E NCI-H929, RPMI-8226, and LP1 cells were treated with the indicated concentration of anlotinib for 24 h or 5 μM anlotinib for the indicated time. Whole cell lysates were subjected to western blotting using c-Myc and β-actin antibodies. Con control group, Anlo anlotinib group. The experiments were performed in triplicate.

Article Snippet: Anlotinib, CHX and MG-132 were purchased from CSNpharm (Chicago, IL, USA), dissolved in Dimethyl Sulfoxide (Sigma, St. Louis, MO) and stored in dark at −20 °C until use.

Techniques: Control, Western Blot, Concentration Assay

Journal: Cell Death & Disease

Article Title: Directly targeting c-Myc contributes to the anti-multiple myeloma effect of anlotinib

doi: 10.1038/s41419-021-03685-w

Figure Lengend Snippet: A NCI-H929 cells were treated with CHX (10 μg/ml) in the presence or absence of anlotinib (5 μM) for the indicated time. The levels of c-Myc protein were evaluated and plotted in the graph. B NCI-H929 and RPMI-8226 cells were treated with either anlotinib (5 μM) and/or MG132 (5 μM) for 6 h, and then the c-Myc protein was assessed by western blotting. C NCI-H929 cells were pretreated with 5 μM MG132 for 3 h and then incubated with 5 μM anlotinib for 3 h. The cell lysates were immunoprecipitated with anti-c-Myc antibody and then probed with anti-ubiquitin antibody. D , E The binding between anlotinib and c-Myc protein was examined by the CETSA method at different temperatures or doses. The indicated proteins were evaluated by western blotting (left). CETSA curves of c-Myc were determined in the absence and presence of anlotinib. Each band intensity of c-Myc in DMSO or anlotinib group was normalized with respect to that obtained at the lowest temperature or dose (right). F Whole cell lysates of NCI-H929 cells were incubated with anlotinib followed by digestion with pronase according to the “Materials and methods” section. Then, the degree of c-Myc degradation was determined by western blot. G , H Overexpression and shRNA knockdown efficiency of c-Myc in NCI-H929 cells was measured by western blotting analysis. The effects of c-Myc knockdown or overexpression on cell apoptosis were evaluated by flow cytometry. The presented columns are given as the means ± SD. Statistically significant values compared with the DMSO group or empty vector group are depicted by * or # , respectively. *** P < 0.001, # P < 0.05, and ### P < 0.001. Con control group, Anlo anlotinib group. Data are shown as mean ± SD and representative of three independent experiments.

Article Snippet: Anlotinib, CHX and MG-132 were purchased from CSNpharm (Chicago, IL, USA), dissolved in Dimethyl Sulfoxide (Sigma, St. Louis, MO) and stored in dark at −20 °C until use.

Techniques: Western Blot, Incubation, Immunoprecipitation, Ubiquitin Proteomics, Binding Assay, Over Expression, shRNA, Knockdown, Flow Cytometry, Plasmid Preparation, Control

Journal: Cell Death & Disease

Article Title: Directly targeting c-Myc contributes to the anti-multiple myeloma effect of anlotinib

doi: 10.1038/s41419-021-03685-w

Figure Lengend Snippet: A NCI-H929, NCI-H929-BR, MM.1S, and MM.1S-BR cells were treated with various concentrations of bortezomib for 24 h. Cell viability was measured by CCK8 assay. B NCI-H929-BR and MM.1S-BR cells were treated with anlotinib (0–20 µM) for 24 and 48 h, followed by an assessment of cell viability. C NCI-H929-BR and MM.1S-BR cells were treated with 5 µM anlotinib for 8 h. The cell cycle was analyzed by flow cytometry. D The morphology of NCI-H929-BR and MM.1S-BR cells after anlotinib treatment (5 μM, 8 h) was observed using Wright staining. E Apoptosis of cells treated with 5 µM anlotinib for 24 h was detected by flow cytometry using Annexin V/PI staining. F NCI-H929-BR and MM.1S-BR cells were treated with anlotinib (5 μM) for the indicated time. Whole cell lysates were subjected to western blotting. G The combined effects of anlotinib and bortezomib in NCI-H929 cells were assessed using the CompuSyn software. Con: control group; Anlo: anlotinib group. *** P < 0.001. Each experiment was performed in triplicate.

Article Snippet: Anlotinib, CHX and MG-132 were purchased from CSNpharm (Chicago, IL, USA), dissolved in Dimethyl Sulfoxide (Sigma, St. Louis, MO) and stored in dark at −20 °C until use.

Techniques: CCK-8 Assay, Flow Cytometry, Wright Stain, Staining, Western Blot, Software, Control

Journal: Cell Death & Disease

Article Title: Directly targeting c-Myc contributes to the anti-multiple myeloma effect of anlotinib

doi: 10.1038/s41419-021-03685-w

Figure Lengend Snippet: A Nude mice bearing subcutaneous NCI-H929 tumors were treated with either anlotinib (3 mg/kg) or vehicle control by intragastric administration for consecutive 14 days. Tumor size was measured every 2 days. B The tumor tissues were excised and weighed on day 14. C Gross appearance of the tumors. D The weight of mice was monitored every 2 days. E Representative IHC staining of tumor tissues. Scale bars: 50 μM. F Tumor tissues were lysed and subjected to western blotting to detect the protein level of c-Myc. Con control group, Anlo anlotinib group. ** P < 0.01, *** P < 0.001.

Article Snippet: Anlotinib, CHX and MG-132 were purchased from CSNpharm (Chicago, IL, USA), dissolved in Dimethyl Sulfoxide (Sigma, St. Louis, MO) and stored in dark at −20 °C until use.

Techniques: Control, Immunohistochemistry, Western Blot

Journal: Canadian Respiratory Journal

Article Title: Anlotinib Inhibits Cisplatin Resistance in Non-Small-Cell Lung Cancer Cells by Inhibiting MCL-1 Expression via MET/STAT3/Akt Pathway

doi: 10.1155/2024/2632014

Figure Lengend Snippet: Anlotinib regulates DDP resistance in NSCLC cells. (a) The viability of A549, A549/DDP, H1299, and H1299/DDP cells under different concentrations of DDP was analyzed by using the CCK8 assay to assess the IC50 value for DDP in cells. (b) Cell viability was detected by using the CCK8 assay under different concentrations of anlotinib to assess the IC50 value for anlotinib in A549/DDP and H1299/DDP cells. (c, d) A549/DDP and H1299/DDP cells were treated with 1 μ M anlotinib, 2 μ M DDP, or 1 μ M anlotinib + 2 μ M DDP. (c) Cell viability was measured by using the CCK8 assay. (d) Colony formation assay was used to assess A549/DDP and H1299/DDP cell proliferation. ∗∗ P < 0.01, ∗∗∗ P < 0.001.

Article Snippet: 24 h later, cells were treated with 1 μ M anlotinib, 2 μ M DDP, or 20 μ M ACT001 (Accendatech Co., Ltd., Tianjin, China) for 24 h.

Techniques: CCK-8 Assay, Colony Assay

Journal: Canadian Respiratory Journal

Article Title: Anlotinib Inhibits Cisplatin Resistance in Non-Small-Cell Lung Cancer Cells by Inhibiting MCL-1 Expression via MET/STAT3/Akt Pathway

doi: 10.1155/2024/2632014

Figure Lengend Snippet: Anlotinib inhibited MET to participate in the DDP resistance of NSCLC cells. (a) MET mRNA expression was detected by qRT-PCR in A549/DDP and H1299/DDP cells treated with or without anlotinib. (b) The p-MET/MET protein expression was examined by western blot analysis in A549/DDP and H1299/DDP cells treated with or without anlotinib. (c–g) A549/DDP and H1299/DDP cells were transfected with oe-MET and then treated with anlotinib and DDP. (c) MET mRNA expression was examined by qRT-PCR. (d) Western blot analysis was used to examine p-MET/MET protein expression. CCK8 assay (e), colony formation assay (f), and transwell assay (g) were used to assess cell viability, proliferation, migration, and invasion. ∗ P < 0.05, ∗∗ P < 0.01, and ∗∗∗ P < 0.001.

Article Snippet: 24 h later, cells were treated with 1 μ M anlotinib, 2 μ M DDP, or 20 μ M ACT001 (Accendatech Co., Ltd., Tianjin, China) for 24 h.

Techniques: Expressing, Quantitative RT-PCR, Western Blot, Transfection, CCK-8 Assay, Colony Assay, Transwell Assay, Migration

Journal: Canadian Respiratory Journal

Article Title: Anlotinib Inhibits Cisplatin Resistance in Non-Small-Cell Lung Cancer Cells by Inhibiting MCL-1 Expression via MET/STAT3/Akt Pathway

doi: 10.1155/2024/2632014

Figure Lengend Snippet: Effects of oe-MET and shMCL-1 on anlotinib-mediated DDP resistance in NSCLC cells. (a, b) A549/DDP and H1299/DDP cells were treated with 1 μ M anlotinib, 2 μ M DDP, or 1 μ M anlotinib+2 μ M DDP. (a) MET and MCL-1 mRNA expression was determined by qRT-PCR. (b) The p-MET/MET and MCL-1 protein expression was examined by western blot analysis. (c–g) A549/DDP and H1299/DDP cells were transfected with oe-MET-1 and sh-MCL-1, followed by treatment with 1 μ M anlotinib and 2 μ M DDP. (c) qRT-PCR was performed to examine MET and MCL-1 mRNA expression. (d) Western blot analysis was carried out to detect p-MET/MET and MCL-1 protein expression. Cell viability, proliferation, migration, and invasion were evaluated using the CCK8 assay (e), colony formation assay (f), and transwell assay (g). ∗ P < 0.05, ∗∗ P < 0.01, and ∗∗∗ P < 0.001.

Article Snippet: 24 h later, cells were treated with 1 μ M anlotinib, 2 μ M DDP, or 20 μ M ACT001 (Accendatech Co., Ltd., Tianjin, China) for 24 h.

Techniques: Expressing, Quantitative RT-PCR, Western Blot, Transfection, Migration, CCK-8 Assay, Colony Assay, Transwell Assay

Journal: Canadian Respiratory Journal

Article Title: Anlotinib Inhibits Cisplatin Resistance in Non-Small-Cell Lung Cancer Cells by Inhibiting MCL-1 Expression via MET/STAT3/Akt Pathway

doi: 10.1155/2024/2632014

Figure Lengend Snippet: Effects of oe-MET and ACT001 on anlotinib-mediated DDP resistance in NSCLC cells. A549/DDP and H1299/DDP cells were transfected with oe-MET-1 and then treated with anlotinib, DDP, and ACT001. (a) The mRNA expression levels of MET and MCL-1 were assessed by qRT-PCR. (b) The protein levels of p-MET/MET, p-STAT3/STAT3, p-Akt/Akt, and MCL-1 were measured by western blot analysis. CCK8 assay (c), colony formation assay (d), and transwell assay (e) were performed to examine cell viability, proliferation, migration, and invasion. ∗∗ P < 0.01 and ∗∗∗ P < 0.001.

Article Snippet: 24 h later, cells were treated with 1 μ M anlotinib, 2 μ M DDP, or 20 μ M ACT001 (Accendatech Co., Ltd., Tianjin, China) for 24 h.

Techniques: Transfection, Expressing, Quantitative RT-PCR, Western Blot, CCK-8 Assay, Colony Assay, Transwell Assay, Migration