Correlation between FAK and EGF-Induced EMT in Colorectal Cancer Cells

Huang, Kun; Gao, Ningning; Bian, Donglin; Zhai, Qixi; Yang, Puxu; Li, Mingwei; Wang, Xuemei

doi:10.1155/2020/5428920

Cited by 32 publications

(19 citation statements)

References 28 publications

(27 reference statements)

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“…E-cadherin, α-SMA and vimentin played important roles in EMT process (40). Huang K et al has revealed that activation of TGF-β signaling could enhance the EMT process (41). Our results were consistent to these findings, suggesting that TGF-β signaling could promote EMT process during the fibrosis.…”

Section: Discussionsupporting

confidence: 90%

Knockdown of lncRNA LINC01234 Suppresses The Tumorigenesis of Liver Cancer via Sponging miR-513a-5p

Song

et al. 2020

Preprint

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Background: Liver cancer is a frequent malignancy with poor prognosis. It has been reported that many lncRNAs could regulate the progression of liver cancer. To identify potential therapeutic targets for liver cancer, we conducted bioinformatics analysis of lncRNAs in tumor tissues and adjacent normal tissues. Methods: The differential expression of lncRNAs between liver cancer tissues and adjacent normal tissues were examined by bioinformatics analysis. Cell proliferation was tested by CCK-8. Cell apoptosis in liver cancer was detected by flow cytometry. Gene and protein expression in liver cancer cells were measured by q-PCR and Western-blot, respectively. Xenograft tumor model was established to verify the function of LINC01234 on liver cancer in vivo.Results: LINC01234 was found to be notably upregulated in liver cancer tissues. In addition, knockdown of LINC01234 significantly inhibited the proliferation, invasion and induced the apoptosis of liver cancer cells. Meanwhile, miR-513a-5p was a downstream target of LINC01234 and USP4 was a direct target of miR-513a-5p. Moreover, downregulation of LINC01234 inhibited the tumorigenesis of liver cancer via inactivating TGF-β signaling.Conclusion: Downregulation of LINC01234 could inhibit the progression of liver cancer. Thus, LINC01234 may serve as a potential novel target for treatment of liver cancer.

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Section: Discussionsupporting

confidence: 90%

Knockdown of lncRNA LINC01234 Suppresses The Tumorigenesis of Liver Cancer via Sponging miR-513a-5p

Song

et al. 2020

Preprint

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“…Similar studies exploring the roles of JAK-STAT signaling and induction of EMT and cancer stemness have been demonstrated for hematopoietic cancers (Wingelhofer et al, 2018), oral squamous cell carcinoma (Chen et al, 2020), and colon cancers (Park et al, 2019b), among others. The role of EMT effectors (Snail, Slug among others) on EMT core regulators (Vimentin, E-cadherin, and N-cadherin) through modulation of various signaling pathways and epigenetic regulation of EMT effectors has been discussed previously (Vu and Datta, 2017;Huang et al, 2020). However, the role of ENC1 as a modulator of EMT effectors and stemness via the JAK-STAT pathway has not been reported previously.…”

Section: Discussionmentioning

confidence: 99%

ENC1 Facilitates Colorectal Carcinoma Tumorigenesis and Metastasis via JAK2/STAT5/AKT Axis-Mediated Epithelial Mesenchymal Transition and Stemness

Cui

Yang

Bai

et al. 2021

Front. Cell Dev. Biol.

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Ectodermal neural cortex 1 (ENC1) is an actin-binding protein and has been known to be upregulated in several cancers, but the molecular mechanisms through which it contributes to the pathology of CRC have largely been elusive. We utilized data mining and validated the aberrant expression of ENC1, following which phenotypic traits of malignancy were assessed in vitro. Ruxolitinib was used as a surrogate to compare the effects of ENC1 expression and silencing on the JAK-STAT-AKT pathway. In vivo models were employed to confirm the in vitro observations. Computation analysis, strengthened by in situ and in vitro data, confirmed the overexpression of ENC1 in CRC and predicted a poor prognosis, while enhanced cell proliferation, invasion, migration, EMT, and stemness were associated with ENC1 overexpression. Silencing of ENC1 downregulated the phenotypes. Additionally, silencing of ENC1 significantly reduced the activation of JAK2 and consequent activation of STAT5 and AKT comparable to ruxolitinib inhibition of JAK2. Silencing of ENC1 resulted in lesser tumor volumes and fewer numbers of tumors, in vivo. These data suggest that ENC1 induces CRC through the JAK2-STAT5-AKT axis. ENC1 is a suitable diagnostic marker for CRC detection, and ENC1 targeting therapies may suppress CRC progression.

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“…The data presented in Figure 8 E depicted that all retinoids were able to significantly reduce the gene expression of IGF1-R and TGF-β1 to the minimal levels. On the other side, recent studies correlate the morphological and phenotypic EMT-like changes with the down-regulation of the epithelial marker E-cadherin [ 46 , 47 , 48 ]. E-cadherin gene was over-expressed in both EC19 and EC23-treated Caco-2 cells with 54- and 16.3- fold changes, respectively.…”

Section: Resultsmentioning

confidence: 99%

Revealing the Potential Application of EC-Synthetic Retinoid Analogues in Anticancer Therapy

et al. 2021

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(1) Background and Aim: All-trans retinoic acid (ATRA) induces differentiation and inhibits growth of many cancer cells. However, resistance develops rapidly prompting the urgent need for new synthetic and potent derivatives. EC19 and EC23 are two synthetic retinoids with potent stem cell neuro-differentiation activity. Here, these compounds were screened for their in vitro antiproliferative and cytotoxic activity using an array of different cancer cell lines. (2) Methods: MTT (3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide) assay, AV/PI (annexin V-fluorescein isothiocyanate (FITC)/propidium iodide (PI)), cell cycle analysis, immunocytochemistry, gene expression analysis, Western blotting, measurement of glutamate and total antioxidant concentrations were recruited. (3) Results: HepG2, Caco-2, and MCF-7 were the most sensitive cell lines; HepG2 (ATRA; 36.2, EC19; 42.2 and EC23; 0.74 µM), Caco-2 (ATRA; 58.0, EC19; 10.8 and EC23; 14.7 µM) and MCF-7 (ATRA; 99.0, EC19; 9.4 and EC23; 5.56 µM). Caco-2 cells were selected for further biochemical investigations. Isobologram analysis revealed the combined synergistic effects with 5-fluorouracil with substantial reduction in IC50. All retinoids induced apoptosis but EC19 had higher potency, with significant cell cycle arrest at subG0-G1, -S and G2/M phases, than ATRA and EC23. Moreover, EC19 reduced cellular metastasis in a transwell invasion assay due to overexpression of E-cadherin, retinoic acid-induced 2 (RAI2) and Werner (WRN) genes. (4) Conclusion: The present study suggests that EC-synthetic retinoids, particularly EC19, can be effective, alone or in combinations, for potential anticancer activity to colorectal cancer. Further in vivo studies are recommended to pave the way for clinical applications.

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Correlation between FAK and EGF-Induced EMT in Colorectal Cancer Cells

Cited by 32 publications

References 28 publications

Knockdown of lncRNA LINC01234 Suppresses The Tumorigenesis of Liver Cancer via Sponging miR-513a-5p

Knockdown of lncRNA LINC01234 Suppresses The Tumorigenesis of Liver Cancer via Sponging miR-513a-5p

ENC1 Facilitates Colorectal Carcinoma Tumorigenesis and Metastasis via JAK2/STAT5/AKT Axis-Mediated Epithelial Mesenchymal Transition and Stemness

Revealing the Potential Application of EC-Synthetic Retinoid Analogues in Anticancer Therapy

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