alpha-solanine and Neoplasm-Metastasis

Solanum nigrum L. (Longkui) is one the most widely used anticancer herbs in traditional Chinese medicine. α‑Solanine is an important ingredient of S. nigrum L. and has demonstrated anticancer properties in various types of cancer. However, the effects of α‑solanine on colorectal cancer remain elusive. The aim of the present study was to assess the effects of α‑solanine on human colorectal cancer cells. The results demonstrated that α‑solanine inhibited the proliferation of RKO cells in a dose‑ and time‑dependent manner. In addition, α‑solanine arrested the cell cycle at the G0/G1 phase and suppressed the expression levels of cyclin D1 and cyclin‑dependent kinase 2 in RKO cells. α‑Solanine induced apoptosis of RKO cells, as indicated by morphological changes and positive Annexin‑FITC/propidium iodide staining. Additionally, α‑solanine activated caspase‑3, ‑8 and ‑9 in RKO cells, which contributed to α‑solanine‑induced apoptosis. α‑Solanine also increased the generation of reactive oxygen species, which contributed to caspase activation and induction of apoptosis. α‑Solanine inhibited the migration, invasion and adhesion of RKO cells, as well as the expression levels and activity of matrix metalloproteinase (MMP)‑2 and MMP‑9. In addition, α‑solanine inhibited cell proliferation, activated caspase‑3, ‑8 and ‑9, induced apoptosis, and inhibited the migration and invasion of HCT‑116 cells. Furthermore, α‑solanine inhibited tumor growth and induced apoptosis in vivo. These findings demonstrated that α‑solanine effectively suppressed the growth and metastatic potential of human colorectal cancer.

Topics: Animals; Antineoplastic Agents; Cell Cycle Checkpoints; Cell Line, Tumor; Cell Movement; Cell Proliferation; Colorectal Neoplasms; Cyclin D1; Cyclin-Dependent Kinase 2; Dose-Response Relationship, Drug; Down-Regulation; Gene Expression Regulation, Neoplastic; HCT116 Cells; Humans; Male; Mice; Neoplasm Metastasis; Solanine; Time Factors; Xenograft Model Antitumor Assays

α-solanine, a steroidal glycoalkaloid in potato, was found to have proliferation-inhibiting and apoptosis-promoting effect on multiple cancer cells, such as clone, liver, melanoma cancer cells. However, the antitumor efficacy of α-solanine on pancreatic cancer has not been fully evaluated. In this study, we inquired into the anti-carcinogenic effect of α-solanine against human pancreatic cancer cells. In the present study, we investigated the anti-carcinogenic effect of α-solanine against human pancreatic cancer cells. In vitro, α-solanine inhibited proliferation of PANC-1, sw1990, MIA PaCa-2 cells in a dose-dependent manner, as well as cell migration and invasion with atoxic doses. The expression of MMP-2/9, extracellular inducer of matrix metalloproteinase (EMMPRIN), CD44, eNOS and E-cadherin were suppressed by α-solanine in PANC-1 cells. Moreover, significantly decreased vascular endothelial growth factor (VEGF) expression and tube formation of endothelial cells were discerned following α-solanine treatment. Suppressed phosphorylation of Akt, mTOR, and Stat3, and strengthen phosphorylation of β-catenin was found, along with markedly decreased tran-nuclear of NF-κB, β-catenin and TCF-1. Following the administration of α-solanine (6 µg/g for 2 weeks) in xenograft model, tumor volume and weight were decreased by 61% and 43% (p<0.05) respectively, showing decreased MMP-2/9, PCNA and VEGF expression. In conclusion, α-solanine showed beneficial effects on pancreatic cancer in vitro and in vivo, which may via suppressing the pathway proliferation, angiogenesis and metastasis.

Topics: Animals; Antineoplastic Agents, Phytogenic; Apoptosis; Cell Line, Tumor; Cell Proliferation; Gene Expression Regulation, Neoplastic; Humans; Mice; Mice, Nude; Neoplasm Metastasis; Neoplasm Proteins; Neovascularization, Pathologic; Pancreatic Neoplasms; Solanine; Xenograft Model Antitumor Assays

Alpha-solanine, a naturally steroidal glycoalkaloid, is found in leaves and fruits of plants as a defensive agent against fungi, bacteria and insects. Herein, we investigated solanine toxicity in vitro and in vivo, and assessed its protective and the therapeutic effects on a typical animal model of breast cancer. The study conducted in three series of experiments to obtain (i) solanine effects on cell viability of mammary carcinoma cells, (ii) in vivo toxicity of solanine, and (iv) the protective and therapeutic effects of solanine on animal model of breast cancer. Alpha-solanine significantly suppressed proliferation of mouse mammary carcinoma cells both in vitro and in vivo (P<0.05). Under the dosing procedure, 5 mg/kg solanine has been chosen for assessing its protective and therapeutic effects in mice breast cancer. Tumor take rate in the solanine-treated group was zero compared with a 75% rate in its respective control group (P<0.05). The average tumor size and weight were significantly lower in solanine-treated animals than its respective control ones (P<0.05). Proapoptotic Bax protein expression increased in breast tumor by solanine compared with its respective control group (P<0.05). Antiapoptotic Bcl-2 protein expression found to be lower in solanine-treated animals (P<0.05). Proliferative and angiogenic parameters greatly decreased in solanine-treated mice (P<0.05). Data provide evidence that solanine exerts a significant chemoprotective and chemotherapeutic effects on an animal model of breast cancer through apoptosis induction, cell proliferation and angiogenesis inhibition. These findings reveal a new therapeutic potential for solanine in cancer.

Topics: Animals; Antineoplastic Agents; Apoptosis; Cell Line, Tumor; Cell Proliferation; Dose-Response Relationship, Drug; Female; Humans; Mammary Neoplasms, Experimental; Mice; Neoplasm Metastasis; Neovascularization, Pathologic; Solanine