APOPTOSIS INDUCTION OF CENTELLA ASIATICA ON HUMAN BREAST CANCER CELLS

The present study evaluated the ability of methanolic extract of Centella asiatica (Linn) Urban (Umbelliferae) to induce apoptosis in different cancer cell lines. MCF-7 cells emerged as the most sensitive cell line for in vitro growth inhibitory activity. C. asiatica extract induced apoptosis in MCF-7 cells as indicated by nuclear condensation, increased annexin staining, loss of mitochondrial membrane potential and induction of DNA breaks identified by TUNEL reactivity. It is possible that the use of C. asiatica extract as a component in herbal medicines could be justifiable

Targeting tumor-associated macrophages by anti-tumor Chinese materia medica

Tumor-associated macrophages (TAMs) play a key role in all stages of tumorigenesis and tumor progression. TAMs secrete different kinds of cytokines, chemokines, and enzymes to affect the progression, metastasis, and resistance to therapy depending on their state of reprogramming. Therapeutic benefit in targeting TAMs suggests that macrophages are attractive targets for cancer treatment. Chinese materia medica (CMM) is an important approach for treating cancer in China and in the Asian region. According to the theory of Chinese medicine (CM) and its practice, some prescriptions of CM regulate the body's internal environment possibly including the remodeling the tumor microenvironment (TME). Here we briefly summarize the pivotal effects of TAMs in shaping the TME and promoting tumorigenesis, invasion, metastasis and immunosuppression. Furthermore, we illustrate the effects and mechanisms of CMM targeting TAMs in antitumor therapy. Finally, we reveal the CMM's dual-regulatory and multi-targeting functions on regulating TAMs, and hopefully, provide the theoretical basis for CMM clinical practice related to cancer therapy

Supplementary Material for: Aloe Emodin Induces G2/M Cell Cycle Arrest and Apoptosis via Activation of Caspase-6 in Human Colon Cancer Cells

Aloe emodin (AE), a natural anthraquinone, is reported to have antiproliferative activity in various cancer cell lines. In this study, we analyzed the molecular mechanisms involved in the growth-inhibitory activity of this hydroxyanthraquinone in colon cancer cell, WiDr. In our observation AE inhibited cell proliferation by arresting the cell cycle at the G2/M phase and inhibiting cyclin B1. AE appreciably induced cell death specifically through the induction of apoptosis and by activating caspases 9/6. Apoptotic execution was found to be solely dependent on caspase-6 rather than caspase-3 or caspase-7. This is the first study indicating that the AE induces apoptosis specifically through the activation of caspase-6

Supplementary Figures S1 - S15 from Obesity-Induced Inflammation and Desmoplasia Promote Pancreatic Cancer Progression and Resistance to Chemotherapy

Supplementary Figures S1 - S15. Supplementary Figure S1. Effect of obesity on tumor initiation. Supplementary Figure S2. Adipose tissue - tumor interaction. Supplementary Figure S3. Correlation of collagen-I levels with tumor size, co-expression of collagen-I and hyaluronan in PSCs, and impact of obesity on desmoplasia and tumor hyaluronan levels. Supplementary Figure S4. Additional Western blotting data from PAN02 tumors. Supplementary Figure S5. Additional effects of AT-1 inhibition on obesity-aggravated desmoplasia, perfusion and drug delivery. Supplementary Figure S6. Additional data on the effect of obesity on immune cell infiltration in tumors. Supplementary Figure S7. Effects of TAN depletion on vessel perfusion in obese mice. Supplementary Figure S8. Effect of obesity on cytokine profile in AK4.4 tumors. Supplementary Figure S9. Effects of TAN depletion on tumor cytokine expression in obese mice. Supplementary Figure S10. Additional effects of losartan on the tumor immune microenvironment. Supplementary Figure S11. Distribution of PDAC patients according to their BMI. Supplementary Figure S12. Effect of obesity on the expression of AT1, Ly6g, and AT1/Ly6g double positivity in PAN02 tumors. Supplementary Figure S13. Representative picture of AT1 expression in cancer-associated adipocytes (arrows) in PAN02 tumors. Supplementary Figure S14. Additional effects of AT1 inhibition on obesity-aggravated microenvironment. Supplementary Figure S15. Prevalance of hypertesion in PDAC patients.</p

Supplementary Tables S1 - S6 from Obesity-Induced Inflammation and Desmoplasia Promote Pancreatic Cancer Progression and Resistance to Chemotherapy

Supplementary Tables S1 - S6. Supplementary Table S1. CT values for demosplasia-related genes in PAN02 tumors. Data obtained from PCR array. Supplementary Table S2. CT values for demosplasia-related genes in AK4.4 tumors. Data obtained from PCR array. Supplementary Table S3. Univariate analysis of prognostic factors for resected pancreatic cancer patients with body mass index (BMI) {less than or equal to}25. Supplementary Table S4. Multivariate analysis of prognostic factors for resected pancreatic cancer patients with body mass index (BMI) {less than or equal to}25. Supplementary Table S5. Univariate analysis of prognostic factors for resected pancreatic cancer patients with body mass index (BMI) >25. Supplementary Table S6. Multivariate analysis of prognostic factors for resected pancreatic cancer patients with body mass index (BMI) >25.</p

Supplementary Methods from Obesity-Induced Inflammation and Desmoplasia Promote Pancreatic Cancer Progression and Resistance to Chemotherapy

Supplementary Methods</p

An anthraquinone derivative, emodin sensitizes hepatocellular carcinoma cells to TRAIL induced apoptosis through the induction of death receptors and downregulation of cell survival proteins

10.1007/s10495-013-0851-5Apoptosis18101175-1187APOP