Additional file 1 of Dynamic altruistic cooperation within breast tumors
Creators: name: Masroni, Muhammad Sufyan Bin
name: Lee, Kee Wah
name: Lee, Victor Kwan Min
name: Ng, Siok Bian
name: Law, Chao Teng
name: Poon, Kok Siong
name: Lee, Bernett Teck-Kwong
name: Liu, Zhehao
name: Tan, Yuen Peng
name: Chng, Wee Ling
name: Tucker, Steven
name: Ngo, Lynette Su-Mien
name: Yip, George Wai Cheong
name: Nga, Min En
name: Hue, Susan Swee Shan
name: Putti, Thomas Choudary
name: Bay, Boon Huat
name: Lin, Qingsong
name: Zhou, Lihan
name: Hartman, Mikael
name: Loh, Tze Ping
name: Lakshmanan, Manikandan
name: Lee, Sook Yee
name: Tergaonkar, Vinay
name: Chua, Huiwen
name: Lee, Adeline Voon Hui
name: Yeo, Eric Yew Meng
name: Li, Mo-Huang
name: Chang, Chan Fong
name: Kee, Zizheng
name: Tan, Karen Mei-Ling
name: Tan, Soo Yong
name: Koay, Evelyn Siew-Chuan
name: Archetti, Marco
name: Leong, Sai Mun
Publisher: name: figshare
Year: 2023
Subjects: subject: Cell Biology
subject: Genetics
subject: FOS: Biological sciences
subject: Molecular Biology
subject: Pharmacology
subject: Biological Sciences not elsewhere classified
subject: Cancer
subject: Infectious Diseases
subject: FOS: Health sciences

description: Additional file 1: Supplementary Note 1. Definition of altruism. Supplementary Note 2. Modeling based on evolutionary game theory predicts persistence of altruistic subpopulation. Supplementary Note 3. Dynamics in spatially structured populations hints at epigenetic mechanism in mediating persistence of altruists. Fig. R1. Social matrix of interaction. From Hamilton (1964) and West et al. (2006). Fig. R2. Survival of the fittest and the tragedy of the commons within tumors. Fig. R3. Frequency-dependent selection. Fig. R4. Dynamics of altruism. Fig. R5. Estimating the parameters. Fig. R6. The observed saturating effect leads to a stable minority of altruistic cancer cells. Fig. R7. Epigenetic determination enables stable altruism. Fig. R8. Increasing therapy leads to more altruistic cooperation. Fig. R9. Why epigenetic-regulated altruism can persist. Fig. S1. microRNA expression in CTCs from breast cancer patients undergoing taxane treatment. Fig. S2. Heterogeneous expression of miR-125b in patient tumor samples and breast cancer cell lines. Fig. S3. Stratification of breast cancer patients based on expression levels of miR-125b, IGFBP2 and CCL28. Fig. S4. Relative survival analysis of miR-125b-associated behavior of breast cancer cell lines and xenografted tumors. Fig. S5. Mechanism of miR-125b-driven fitness disadvantage of cancer cell altruism. Fig. S6. Mechanism of miR-125b-driven fitness benefit of cancer cell altruism. Fig. S7. Heightened co-expressions of oncogenes and tumor suppressors in miR-125bHigh altruists. Fig. S8. MiR-125bHigh altruists are regenerable via a KLF2-mediated acetylation. Fig. S9. ChIP reveals protein-chromatin interactions at two different KLF2 binding sites. Fig. S10. Lateral inhibition maintains a sparse spatial organization of altruists. Table S1. Clinical characteristics of breast cancer patients for miRNA profiling of CTCs (Supplementary Fig. 1). Table S2. Clinical characteristics of breast cancer patients for miR-125b in-situ hybridization (Fig. 1A) Table S3. Selected results of comparative analysis of RNA-Sequencing of biotinylated miR-125b mimics versus control mimic pulldown (Figs. 2 and 4). Table S4. Results of comparative proteomic analysis of conditioned media from miR-125b or control mimic-transfected MCF7 cells using iTRAQ (Fig. 2H). Table S5. Clinical characteristics of breast cancer patients for detection of IGFBP2 and CCL28 protein levels in plasma (Fig. S6G).