Akt Forma Nt Blank Skachat UPD
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Overexpression of TAZ in the mouse liver triggered iCCA development with very low incidence and long latency. In contrast, co-expression of TAZ and myr-AKT dramatically increased tumor frequency and accelerated cancer formation in mice, with 100% iCCA incidence and high tumor burden by 10 weeks post hydrodynamic injection. AKT/TAZ tumors faithfully recapitulated many of the histomolecular features of human iCCA. At the molecular level, the development of the cholangiocellular lesions depended on the binding of TAZ to TEAD transcription factors. In addition, inhibition of the Notch pathway did not hamper carcinogenesis but suppressed the cholangiocellular phenotype of AKT/TAZ tumors. Also, knockdown of YAP, the TAZ paralog, delayed cholangiocarcinogenesis in AKT/TAZ mice without affecting the tumor phenotype. Furthermore, human preinvasive and invasive iCCAs and mixed hepatocellular carcinoma/iCCA displayed widespread TAZ activation and downregulation of the mechanisms protecting TAZ from proteolysis.
Different from YAP, the available information on the role of TAZ in liver cancer is very limited. TAZ expression significantly correlates with aggressive HCC features, including tumor size, TNM stage, lymph node or distant metastasis, histological differentiation, recurrence, and poor prognosis [28]. Furthermore, forced overexpression of TAZ promotes cell proliferation, migration, and invasion of HCC cell lines in vitro, whereas opposite effects accompany TAZ knockdown [28, 29]. In iCCA, recent studies indicate that TAZ expression is more pronounced in tumor tissues than in the peritumoral counterpart [30, 31]. Also, high levels of TAZ are associated with a lower overall survival rate of iCCA patients after partial liver resection [30]. In addition, the simultaneous expression of TAZ and YAP correlates with chromosomal instability in this tumor type [32].
Liver specimens were harvested and fixed in 10% formalin overnight at 4C and embedded in paraffin. Hematoxylin and eosin (ThermoFisher Scientific, Waltham, MA) staining was conducted using a standard protocol on human and mouse liver sections. Subsequently, the slides were analyzed by three expert liver pathologists (SR, ME, and KE) in a blinded fashion and according to the criteria established by Frith and Ward [36]. Immunohistochemistry (IHC) was performed as described [25]. The primary antibodies used in the study are reported in Table 1.
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The levels of AFP and ALT in serum of DEN-induced rats. The concentration of AFP (A) and ALT (B) in the serum of DEN-induced rats. All data were expressed as mean SD, n = 6. * p C), control group was untreated HepG2 cells; OB was Oroxin B group; The micRNA-221 expression in DEN-induced rats liver tissues (D), blank group was not administered group, control group was DEN-induced group, OBH was OB high-dose group, OBM was OB medium-dose group, OBL was OB low-dose group. The levels of miR-221 was detected by RT-PCR and measured with U6 as an internal reference. All data were expressed as mean SD, n = 6. ** p
Knockdown of MACC1 markedly inhibited the stemness of CC cells. (a) Representative images showing the spheroid formation ability of Caski and C-33A cells after transfection with non-target siRNA (NT) or MACC1 siRNAs. (b) Western blot and (c) qRT-PCR were used to assess protein and mRNA expression levels of stemness markers (OCT4 and Nanog) in MACC1-knockdown Caski and C-33A cells. (d) After MACC1 knockdown by siRNAs, protein expression levels of p-AKT and p-STAT3 were confirmed by Western blot in Caski and C-33A cells
Colivelin could reverse the inhibition of MACC1 knockdown on stemness in CC cells. (a) Representative images showing the influence of MACC1 knockdown or/and Colivelin exposure on the spheroid formation abilities of Caski and C-33A cells. (b-c) MACC1-knockdown Caski and C-33A cells were treated with Colivelin. Then Western blot (b) and qRT-PCR (c) were used to assess protein and mRNA expression levels of stemness markers (OCT4 and Nanog) (d) Protein expression levels of p-AKT and p-STAT3 were identified through Western blotting analysis in Caski and C-33A cells that were co-treated with MACC1 siRNAs and Colivelin
Adenomyoepithelioma of the breast is a rare biphasic tumor composed of epithelial and myoepithelial cells1, which typically displays a benign clinical course, but may recur locally2 and/or metastasize3. Phenotypically, adenomyoepitheliomas are heterogeneous. The epithelial component may express estrogen receptor (ER) and progesterone receptor (PR); however, a subset of adenomyoepitheliomas lacks the expression of hormone receptors altogether1. Both the epithelial and myoepithelial compartments can expand and undergo malignant transformation, histologically characterized by nuclear atypia, mitotic activity, and/or necrosis1,2,4. Importantly, however, metastases have been documented even in cases lacking a histologically overt malignant component3. Interestingly, most invasive breast cancers arising in adenomyoepitheliomas display a triple-negative phenotype (ER-, PR- and HER2-negative) and metaplastic features1.
To assess the effects of AKT and MEK inhibition further, we treated EV- or mutant HRASQ61R-expressing MCF-10AP and MCF-10AH1047R cells grown in three-dimensional cultures. AKT and MEK inhibition led to a partial reversion of the phenotypic transformation caused by mutant HRASQ61R expression in MCF-10AP and MCF-10AH1047R cells, which was more overt under treatment with the combination of AKT and MEK inhibitors (Fig. 7d), consistent with the results obtained in monolayer cultures.
Histologic assessment of architectural subtype, necrosis, mitotic rate, nuclear pleomorphism, and associated carcinomas were performed by three pathologists (F.C.G., F.P., and J.R.S.-F.). The architectural subtype was defined as tubular or papillary following previously defined criteria1,2. Necrosis, mitotic rate, and nuclear pleomorphism have been shown to constitute histologic features associated with aggressive behavior and malignant transformation in breast adenomyoepitheliomas1,2. Necrosis was defined as present (any area) or absent. Mitotic rate was defined as the number of mitotic figures in the myoepithelial or epithelial cell compartments per mm2, and stratified into three categories. Nuclear pleomorphism was evaluated according to the Nottingham histologic grading system of breast cancer42. The presence and histologic type of an associated invasive carcinoma in the primary adenomyoepitheliomas and/or recurrent lesions in the ipsilateral breast was assessed according to the WHO criteria2.
B.W. and J.S.R.-F. conceived the study. F.C.G., S.M., M.P.F., H.Y.W., E.B., J.P., B.P.R., Z.V., I.O.E. and E.A.R. provided tissue samples. F.C.G., F.P., M.E., E.A.R., I.O.E. and J.S.R.-F. performed the histopathologic review. F.C.G., A.L., A.D.P., A.S., H.-C.W., S.P., A.M.S., L.G.M., F.P., A.B., D.F., T.B., A.D.C.P, J.L. and A.A.J. carried out the experiments. P.S., K.A.B., R.K. and P.B. performed the bioinformatics analyses, which were coordinated by F.C.G., C.K.Y.N., B.W. and J.S.R.-F. F.C.G., A.L., A.D.P., S.P., A.S., C.K.Y.N., L.G.M., L.N., I.O.E., E.A.R., S.C., B.W. and J.S.R.-F. interpreted the results. F.C.G. and A.L. wrote the first draft, which was initially reviewed by S.C., B.W. and J.S.R.-F. All authors read, edited and approved the final manuscript.
Our results showed that miR-150 overexpression in early EPCs significantly promoted differentiation to ECFCs and contributed to proliferation and tube formation. However, suppression of miR-150 in late EPCs inhibited proliferation and tube formation. Moreover, we identified that this progression is regulated by inhibition of c-Myb and activation of the Akt/FOXO1 pathway. Our findings also showed that miR-150 led to the enhanced resolution ability of EPCs in a rat venous thrombosis model.
As miR-150 levels were significantly different between eEPCs and ECFCs, we hypothesized that differences in gene expression may lead to the functional differences between the two cell types. Overexpression of miR-150 in eEPCs increased EPC formation of tube-like structures compared to eEPCs (Fig. 3a). This phenomenon was consistent with observations from an in vivo Matrigel plug assay (Fig. 3b, c). Furthermore, miR-150 agomir increased the eEPC proliferation compared to control (Fig. 3d). In addition, miR-150 downregulation in ECFCs reduced angiogenesis, and upregulation of miR-150 further promoted angiogenesis and proliferation in ECFCs (Fig. 3a, d). Following an ELISA to test VEGF and IL-8 secretion by EPCs, results showed miR-150 downregulation reduced VEGF and IL-8 production in eEPCs (Fig. 3e, f). Meanwhile, both inhibition and promotion of miR-150 in ECFCs did not influence supernatant VEGF and IL-8 concentrations (Fig. 3e, f). 041b061a72