We are analyzing https://link.springer.com/article/10.1007/s10555-010-9257-9.

Title:
The guardians of the genome (p53, TA-p73, and TA-p63) are regulators of tumor suppressor miRNAs network | Cancer and Metastasis Reviews
Description:
The tumor suppressor p53 homologues, TA-p73, and p63 have been shown to function as tumor suppressors. However, how they function as tumor suppressors remains elusive. Here, I propose a number of tumor suppressor pathways that illustrate how the TA-p73 and p63 could function as negative regulators of invasion, metastasis, and cancer stem cells (CSCs) proliferation. Furthermore, I provide molecular insights into how TA-p73 and p63 could function as tumor suppressors. Remarkably, the guardians—p53, p73, and p63—of the genome are in control of most of the known tumor suppressor miRNAs, tumor suppressor genes, and metastasis suppressors by suppressing c-myc through miR-145/let-7/miR-34/TRIM32/PTEN/FBXW7. In particular, p53 and TA-p73/p63 appear to upregulate the expression of (1) tumor suppressor miRNAs, such as let-7, miR-34, miR-15/16a, miR-145, miR-29, miR-26, miR-30, and miR-146a; (2) tumor suppressor genes, such as PTEN, RBs, CDKN1a/b/c, and CDKN2a/b/c/d; (3) metastasis suppressors, such as Raf kinase inhibitory protein, CycG2, and DEC2, and thereby they enlarge their tumor suppressor network to inhibit tumorigenesis, invasion, angiogenesis, migration, metastasis, and CSCs proliferation.
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Topics {✒️}

nf-kappab-yy1-mir-29 regulatory circuitry founding director-cum-senior scientist tgf-beta-induced collagen expression dleu2/mir-15a/16–1 cluster controls protein-ubiquitin ligase scf c-myc-binding protein antigen-induced t-cell proliferation myc-induced b-cell lymphomas ubiquitin-mediated proteasomal degradation p73-mediated e1a-induced suppression microrna-23b mediates urokinase gsk-3beta-mediated phosphorylation month download article/chapter uncovering growth-suppressive mirnas breast tumor-initiating cells arf-p53-independent cellular senescence p53 represses c-myc pre-mir-146a contribute e2f-1-mediated apoptotic pathways prb-related protein p130 mir-145 induces caspase-dependent brca2-mutant thymic lymphomas bmp-4-induced epidermal commitment myc-modulated mir-9 makes fluorescent methylation-specific pcr trip-br links e2f post-graduate medical education empower tgfbeta-induced metastasis mir-29a suppresses tristetraprolin 7/mir-34/trim32/pten/fbxw7 hormone-refractory prostate cancer myc-activated mirna cluster gil-diez-de-medina hif-1alpha promotes metastasis high-grade bladder cancer myc/mycn-activated mirna double-negative feedback loop trim-nhl proteins activating rho-family gtpases mir-34a inhibits migration n-cadherin/src homology induce epithelial–mesenchymal transition suppressing c-myc transcription factor ets1 tap63alpha induces ap-2gamma tissue-specific stem cells mirna-mrna interactions conserved rna-binding protein e-cadherin promotes metastasis reduced pten protein

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      description:The tumor suppressor p53 homologues, TA-p73, and p63 have been shown to function as tumor suppressors. However, how they function as tumor suppressors remains elusive. Here, I propose a number of tumor suppressor pathways that illustrate how the TA-p73 and p63 could function as negative regulators of invasion, metastasis, and cancer stem cells (CSCs) proliferation. Furthermore, I provide molecular insights into how TA-p73 and p63 could function as tumor suppressors. Remarkably, the guardians—p53, p73, and p63—of the genome are in control of most of the known tumor suppressor miRNAs, tumor suppressor genes, and metastasis suppressors by suppressing c-myc through miR-145/let-7/miR-34/TRIM32/PTEN/FBXW7. In particular, p53 and TA-p73/p63 appear to upregulate the expression of (1) tumor suppressor miRNAs, such as let-7, miR-34, miR-15/16a, miR-145, miR-29, miR-26, miR-30, and miR-146a; (2) tumor suppressor genes, such as PTEN, RBs, CDKN1a/b/c, and CDKN2a/b/c/d; (3) metastasis suppressors, such as Raf kinase inhibitory protein, CycG2, and DEC2, and thereby they enlarge their tumor suppressor network to inhibit tumorigenesis, invasion, angiogenesis, migration, metastasis, and CSCs proliferation.
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         Metastasis
         CSCs
         Cancer Research
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