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  1. Article ; Online: The roles and molecular mechanisms of long non-coding RNA WT1-AS in the maintenance and development of gastric cancer stem cells

    Xiaobei Zhang / Meng Jin / Shiqi Liu / Mingde Zang / Lei Hu / Tao Du / Baogui Zhang

    Heliyon, Vol 9, Iss 4, Pp e14655- (2023)

    2023  

    Abstract: It has been proposed that cancer stem cells (CSCs) are responsible for almost all malignant phenotypes of tumors. Long non-coding RNA WT1 antisense RNA (WT1-AS) has been found to be implicated in lung cancer cell stemness. However, the roles and ... ...

    Abstract It has been proposed that cancer stem cells (CSCs) are responsible for almost all malignant phenotypes of tumors. Long non-coding RNA WT1 antisense RNA (WT1-AS) has been found to be implicated in lung cancer cell stemness. However, the roles and molecular mechanisms of WT1-AS in the development of gastric cancer stem cells (GCSCs) remain unknown. Our present study showed that WT1-AS negatively regulated WT1 expression in GCSCs. WT1-AS knockdown or Wilms’ tumor 1 (WT1) overexpression improved GCSC proliferative and migratory capacities, inhibited GCSC apoptosis, potentiated the resistance of GCSCs to 5-FU, promoted GCSC EMT, induced HUVEC angiogenesis, enhanced GCSC stemness, and facilitated in-vitro 3D GCSC aggregate formation. WT1-AS overexpression exerted reverse effects. WT1-AS ameliorated the malignant phenotypes of GCSCs by down-regulating WT1 in vitro. WT1-AS inhibited tumor growth and metastasis, and reduced tumor stemness in GCSCs-derived (s.c., i.p., and i.v.) xenografts in vivo. Moreover, XBP1 was identified as an upstream regulator of WT1-AS in GCSCs. Also, 4 potential WT1-AS downstream targets (i.e. PSPH, GSTO2, FYN, and PHGDH) in GCSCs were identified. Additionally, CACNA2D1 was demonstrated to be a downstream target of the WT1-AS/WT axis. XBP1 or CACNA2D1 knockdown exerted an adverse effect on the maintenance of stem cell-like behaviors and characteristics of GCSCs. In conclusion, WT1-AS weakened the stem cell-like behaviors and characteristics of GCSCs in vitro and in vivo by down-regulating WT1. Investigations into the molecular mechanisms underlying the complex phenotypes of GCSCs might contribute to the better management of gastric cancer.
    Keywords Gastric cancer stem cells ; Growth ; Metastasis ; WT1-AS ; RNA sequencing ; Science (General) ; Q1-390 ; Social sciences (General) ; H1-99
    Subject code 571
    Language English
    Publishing date 2023-04-01T00:00:00Z
    Publisher Elsevier
    Document type Article ; Online
    Database BASE - Bielefeld Academic Search Engine (life sciences selection)

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  2. Article ; Online: BPTF Drives Gastric Cancer Resistance to EGFR Inhibitor by Epigenetically Regulating the C‐MYC/PLCG1/Perk Axis

    Fangyuan Li / Junxian Yu / Tao Pan / Haoran Feng / Jianfang Li / Beiqin Yu / Zhiyuan Fan / Qingqing Sang / Mengdi Chen / Mingde Zang / Junyi Hou / Xiongyan Wu / Yingyan Yu / Yuan‐Yuan Li / Chao Yan / Zhenggang Zhu / Liping Su / Bingya Liu

    Advanced Science, Vol 10, Iss 34, Pp n/a-n/a (2023)

    2023  

    Abstract: Abstract Erlotinib, an EGFR tyrosine kinase inhibitor, is used for treating patients with cancer exhibiting EGFR overexpression or mutation. However, the response rate of erlotinib is low among patients with gastric cancer (GC). The findings of this ... ...

    Abstract Abstract Erlotinib, an EGFR tyrosine kinase inhibitor, is used for treating patients with cancer exhibiting EGFR overexpression or mutation. However, the response rate of erlotinib is low among patients with gastric cancer (GC). The findings of this study illustrated that the overexpression of bromodomain PHD finger transcription factor (BPTF) is partially responsible for erlotinib resistance in GC, and the combination of the BPTF inhibitor AU‐1 with erlotinib synergistically inhibited tumor growth both in vivo and in vitro. AU‐1 inhibited the epigenetic function of BPTF and decreased the transcriptional activity of c‐MYC on PLCG1 by attenuating chromosome accessibility of the PLCG1 promoter region, thus decreasing the expression of p‐PLCG1 and p‐Erk and eventually improving the sensitivity of GC cells to erlotinib. In patient‐derived xenograft (PDX) models, AU‐1 monotherapy exhibited remarkable tumor‐inhibiting activity and is synergistic anti‐tumor effects when combined with erlotinib. Altogether, the findings illustrate that BPTF affects the responsiveness of GC to erlotinib by epigenetically regulating the c‐MYC/PLCG1/pErk axis, and the combination of BPTF inhibitors and erlotinib is a viable therapeutic approach for GC.
    Keywords AU‐1 ; BPTF ; EGFR‐TKI ; erlotinib ; gastric cancer ; targeted therapy ; Science ; Q
    Subject code 616
    Language English
    Publishing date 2023-12-01T00:00:00Z
    Publisher Wiley
    Document type Article ; Online
    Database BASE - Bielefeld Academic Search Engine (life sciences selection)

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  3. Article ; Online: CEACAM6 promotes gastric cancer invasion and metastasis by inducing epithelial-mesenchymal transition via PI3K/AKT signaling pathway.

    Mingde Zang / Baogui Zhang / Yunqiang Zhang / Jianfang Li / Liping Su / Zhenggang Zhu / Qinlong Gu / Bingya Liu / Min Yan

    PLoS ONE, Vol 9, Iss 11, p e

    2014  Volume 112908

    Abstract: Overexpressed CEACAM6 in tumor tissues plays important roles in invasion, metastasis and anoikis resistance in a variety of human cancers. We recently reported that CEACAM6 expression is upregulated in Gastric cancer (GC) tissues and promoted GC ... ...

    Abstract Overexpressed CEACAM6 in tumor tissues plays important roles in invasion, metastasis and anoikis resistance in a variety of human cancers. We recently reported that CEACAM6 expression is upregulated in Gastric cancer (GC) tissues and promoted GC metastasis. Here, we report that CEACAM6 promotes peritoneal metastases in vivo and is negatively correlated with E-cadherin expression in GC tissues. Overexpressed CEACAM6 induced epithelial-mesenchymal transition (EMT) in GC, as measured by increases in the EMT markers N-cadherin, Vimentin and Slug while E-cadherin expression was decreased in CEACAM6-overexpressing GC cells; opposing results were observed in CEACAM6-silenced cells. Furthermore, E-cadherin expression was negatively correlated with depth of tumor invasion, lymph node metastasis and TNM stage in GC tissues. Additionally, CEACAM6 elevated matrix metalloproteinase-9 (MMP-9) activity in GC, and anti-MMP-9 antibody could reverse the increasing invasion and migration induced by CEACAM6. CEACAM6 also increased the levels of phosphorylated AKT, which is involved in the progression of a variety of human tumors. We further observed that LY294002, a PI3K inhibitor, could reverse CEACAM6-induced EMT via mesenchymal-epithelial transition. These findings suggest that CEACAM6 enhances invasion and metastasis in GC by promoting EMT via the PI3K/AKT signaling pathway.
    Keywords Medicine ; R ; Science ; Q
    Subject code 616
    Language English
    Publishing date 2014-01-01T00:00:00Z
    Publisher Public Library of Science (PLoS)
    Document type Article ; Online
    Database BASE - Bielefeld Academic Search Engine (life sciences selection)

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