Decreased Expression of Caveolin-1 and E-Cadherin Correlates with the Clinicopathologic Features of Gastric Cancer and the EMT Process

Zhang, Kundong; Yang, Guang; Wu, Weidong; Zhang, Jing; Xia, Xiang; Jiang, Tao; Cao, Jun; Huang, Kejan; Qiu, Zhengjun; Huang, Chengdu

doi:10.2174/1574892811666160128151437

Cited by 23 publications

(25 citation statements)

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“…The classical cadherin CDH1 (also known as E-Cadherin) is processed to generate a mature calcium-dependent cell-cell adhesion protein comprised of five extracellular cadherin repeats, a transmembrane region, and a highly conserved cytoplasmic tail. Decreased CDH1 expression is positively correlated with gastric cancer progression [25–27]; the decreased CDH1 (E-Cadherin) expression observed here might partially explain the ability of UBE2T knockdown to attenuate gastric tumor formation and growth. GSK3B (glycogen synthase kinase 3 beta) is a serine-threonine kinase involved in energy metabolism, neuronal cell development [28], inflammation, and osteoporosis [29] that also plays an important role in transcriptional regulation and oncogenic signaling.…”

Section: Discussionmentioning

confidence: 90%

UBE2T knockdown inhibits gastric cancer progression

Luo

Yao

et al. 2017

Oncotarget

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Ubiquitin-conjugating enzymes (E2 enzymes) such as UBE2T target proteins for degradation via the proteasome. Here, we examined the effects of UBE2T on the progression of gastric cancer. UBE2T was highly expressed in gastric tumors and gastric cancer cells. siRNA-mediated suppression of UBE2T inhibited gastric cancer cell proliferation and colony formation by promoting cell cycle arrest at G2/M phase and increasing apoptosis. Suppression of UBE2T also attenuated the invasive and metastatic abilities of gastric cancer cells by altering expression of epithelial-mesenchymal transition (EMT)-related factors. A xenograft model in which nude mice were injected with UBE2T knockdown human gastric cancer cells confirmed that suppression of UBE2T also decreased tumor formation and growth in vivo. Expression levels of CCND1, Phospho-GSK3B, WNT family members, and MYC were all affected by UBE2T knockdown. These results suggest that UBE2T plays a critical role in gastric cancer, and that it may serve as a useful prognostic biomarker and therapeutic target in gastric cancer patients.

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Section: Discussionmentioning

confidence: 90%

UBE2T knockdown inhibits gastric cancer progression

Luo

Yao

et al. 2017

Oncotarget

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“…Recent studies have reported cross-talk between E-cadherin, Caveolin-1, β-catenin and TGF-β signaling [22][23][24][25][26]. Caveolin-1 protein is highly expressed in the K562-IR cell line when compared to K562.…”

Section: Tki-resistant K562-ir Cells Form Tumor Spheroids Express Himentioning

confidence: 99%

Adaptive phenotypic modulations lead to therapy resistance in chronic myeloid leukemia cells

et al. 2020

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Tyrosine kinase inhibitor (TKI) resistance is a major problem in chronic myeloid leukemia (CML). We generated a TKI-resistant K562 sub-population, K562-IR, under selective imatinib-mesylate pressure. K562-IR cells are CD34-/CD38-, BCR-Abl-independent, proliferate slowly, highly adherent and form intact tumor spheroids. Loss of CD45 and other hematopoietic markers reveal these cells have diverged from their hematopoietic origin. CD34 negativity, high expression of E-cadherin and CD44; decreased levels of CD45 and β-catenin do not fully confer with the leukemic stem cell (LSC) phenotype. Expression analyses reveal that K562-IR cells differentially express tissue/organ development and differentiation genes. Our data suggest that the observed phenotypic shift is an adaptive process rendering cells under TKI stress to become oncogene independent. Cells develop transcriptional instability in search for a gene expression framework suitable for new environmental stresses, resulting in an adaptive phenotypic shift in which some cells partially display LSC-like properties. With leukemic/cancer stem cell targeted therapies underway, the difference between treating an entity and a spectrum of dynamic cellular states will have conclusive effects on the outcome.

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“…E-cadherin is the adhesion molecule of epithelial cell surface, and plays an important role in the adhesion between cells (33). The downregulation of E-cadherin is an important feature of EMT (34). Additionally, EMT is a significant cause of tumor invasion and metastasis.…”

Section: Introductionmentioning

confidence: 99%

Annexin A2 inhibition suppresses ovarian cancer progression via regulating β-catenin/EMT

Liu

Ban

et al. 2017

Oncology Reports

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Annexin A2 is a member of the Annexin family that acts as a Ca2+-dependent phospholipid and membrane binding protein, which is associated with the survival and spread of multiple neoplasms. However, the function of Annexin A2 in ovarian cancer progression remains unclear. In this study, we aimed to investigate the role and underlying molecular mechanism of Annexin A2 in cell proliferation and invasion in ovarian cancer. We found that the mRNA expression of Annexin A2 was upregulated in ovarian cancer tissues and cell lines. In the loss-of-function of Annexin A2, β-catenin was indicated to be significantly suppressed and EMT constrained. Moreover, cell proliferation and invasion were both markedly inhibited by the downregulation of Annexin A2. Additionally, the overexpression of β-catenin obviously reversed the effect of Annexin A2 on EMT, and cell proliferation and invasion, indicating that Annexin A2 suppression regulated EMT through controlling β-catenin. Taken together, this study showed that Annexin A2 inhibition suppresses proliferation and invasion in ovarian cancer via β-catenin/EMT, proposing the potential role of Annexin A2 in the prevention and treatment of ovarian cancer.

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Decreased Expression of Caveolin-1 and E-Cadherin Correlates with the Clinicopathologic Features of Gastric Cancer and the EMT Process

Abstract: Decreased expression of Cav-1 and E-cadherin may play an important role in the progression of gastric cancer; Knockdown of Cav-1 may promote EMT of gastric cancer by targeting E-cadherin.

Cited by 23 publications

References 0 publications

UBE2T knockdown inhibits gastric cancer progression

UBE2T knockdown inhibits gastric cancer progression

Adaptive phenotypic modulations lead to therapy resistance in chronic myeloid leukemia cells

Annexin A2 inhibition suppresses ovarian cancer progression via regulating β-catenin/EMT

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