Dihydroartemisinin suppresses proliferation, migration, the Wnt/β‑catenin pathway and EMT via TNKS in gastric cancer

Ma, Yanmei; Zhang, Peng; Zhang, Qilong; Wang, Xiaofei; Miao, Qiong; Lyu, Xiaolan; Cui, Bo; Ma, Honghong

doi:10.3892/ol.2021.12949

Cited by 9 publications

(3 citation statements)

References 44 publications

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“…18 Many cancer studies have demonstrated that β-catenin, N-cadherin, and vimentin are involved in the metastasis of cancer cells, including GC. 19,20 In this study, ADORA2B agonists and antagonists effectively regulated the expression levels of β-catenin, N-cadherin, and vimentin. Additionally, unlike that in GC tissue, ADORA2B expression was elevated in both the nucleus and the cytoplasm of metastatic cells.…”

Section: Discussionmentioning

confidence: 64%

Adenosine Receptor A2B Antagonist Inhibits the Metastasis of Gastric Cancer Cells and Enhances the Efficacy of Cisplatin

Wang

Tan

et al. 2023

Technol Cancer Res Treat

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Adenosine receptors play a key role in cancer progression. This study investigated the effect of the adenosine A2B receptor (ADORA2B) on epithelial–mesenchymal transition (EMT) markers and cell metastasis of gastric cancer (GC) cells. Public databases were used to investigate the specificity of ADORA2B expression in GC tissue. We used immunohistochemistry and immunofluorescence to detect ADORA2B expression in GC tissue, paracancerous tissue, and metastatic greater omental tissue. AGS and HGC-27 GC cells were selected. The effect of ADORA2B on the invasion and migration of GC cells was examined using cell scratch and transwell assays. The effect of ADORA2B on the expression of EMT marker proteins (β-catenin, N-cadherin, and vimentin) in GC cells was measured by cellular immunohistochemistry, immunofluorescence, and Western blot. The effects of an ADORA2B inhibitor combined with cisplatin on EMT markers in GC cells were further explored. The expression levels of ADORA2B in GC tissue, metastatic greater omental tissue, and lymphatic metastasis tissue were significantly higher than those in paracancerous tissue, and ADORA2B was associated with lymph node metastasis and invasion. ADORA2B significantly regulated the invasion and migration ability of GC cells and the expression levels of EMT marker proteins. The combination of an ADORA2B antagonist (PSB-603) and cisplatin had a more significant effect on reversing the expression of EMT marker proteins. ADORA2B was overexpressed in GC tissue, metastatic greater omental tissue, and metastatic lymph node tissue. ADORA2B regulated the expression of EMT marker proteins in GC cells and affected GC cell metastasis. Antagonizing ADORA2B expression increased the efficacy of cisplatin treatment.

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Section: Discussionmentioning

confidence: 64%

Adenosine Receptor A2B Antagonist Inhibits the Metastasis of Gastric Cancer Cells and Enhances the Efficacy of Cisplatin

Wang

Tan

et al. 2023

Technol Cancer Res Treat

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“…DHA inhibits EMT process in gastric cancer by inhibiting Wnt/β-catenin pathway [23][24][25][26] . Additionally, DHA decreases the ability of EC cells to migrate in esophageal cancer by increasing their autophagy [24] .…”

Section: Discussionmentioning

confidence: 99%

Dihydroartemisinin inhibits EMT progression in medullary thyroid carcinoma through Hippo signaling pathway regulated by IL-6

Li,

Zhang,

et al. 2023

Preprint

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Dihydroartemisinin, an artemisinin derivative, has the ability to influence both the inflammatory response and the growth of certain malignancies. In this study, we used the CCK-8 and Transwell assays to show that DHA had a suppressive effect on the growth, migration, and invasion of medullary thyroid cancer cells. Furthermore, we used Elisa, Western blot, and immunofluorescence assays to confirm the expression of transcriptional co-activators YAP/TAZ downstream of the Hippo pathway, as well as changes in the expression of EMT process markers E-cadherin and N-cadherin.The results demonstrated that DHA effectively reduced the expression of IL-6 in medullary thyroid carcinoma cells and hindered their EMT process by regulating the Hippo pathway. This regulation was achieved through the promotion of YAP phosphorylation and the inhibition of YAP/TAZ protein expression.Following additional activation of the Hippo pathway with GA-017, the inhibitory effect of DHA on IL-6 was alleviated. Subsequently, the Hippo pathway was activated, leading to an increase in the expression of E-cadherin, a marker associated with the epithelial-mesenchymal transition (EMT) process. In conclusion, this study demonstrates that DHA can regulate the Hippo pathway by inhibiting IL-6 secretion, leading to the inhibition of the EMT process in medullary thyroid carcinoma. These findings provide a theoretical foundation for further exploring the anticancer mechanism of DHA. Additionally, this study offers valuable insights for the potential clinical application of DHA as a combination drug.

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“…Subsequently, the released β-catenin enters the nucleus to transactivate Wnt target genes 153,154 . TNKS is overexpressed in many cancers, including HCC, gastric cancer, and colorectal cancer [155][156][157] . The TNKS inhibitors XAV939, WXL-8, and NVP-TNKS656, attenuated Wnt/β-catenin signaling and inhibited the growth of HCC cells [157][158][159] (Figure 4).…”

Section: Tankyrasementioning

confidence: 99%

Wnt signaling in liver regeneration, disease, and cancer

Zou¹,

Park²

2023

Clin Mol Hepatol

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The liver exhibits the highest recovery rate from acute injuries. However, in chronic liver disease, the long-term loss of hepatocytes often leads to adverse consequences such as fibrosis, cirrhosis, and liver cancer. The Wnt signaling plays a pivotal role in both liver regeneration and tumorigenesis. Therefore, manipulating the Wnt signaling has become an attractive approach to treating liver disease, including cancer. Nonetheless, given the crucial roles of Wnt signaling in physiological processes, blocking Wnt signaling can also cause several adverse effects. Recent studies have identified cancer-specific regulators of Wnt signaling, which would overcome the limitation of Wnt signaling target approaches. In this review, we discussed the role of Wnt signaling in liver regeneration, precancerous lesion, and liver cancer. Furthermore, we summarized the basic and clinical approaches of Wnt signaling blockade and proposed the therapeutic prospects of cancer-specific Wnt signaling blockade for liver cancer treatment.

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Dihydroartemisinin suppresses proliferation, migration, the Wnt/β‑catenin pathway and EMT via TNKS in gastric cancer

Cited by 9 publications

References 44 publications

Adenosine Receptor A2B Antagonist Inhibits the Metastasis of Gastric Cancer Cells and Enhances the Efficacy of Cisplatin

Adenosine Receptor A2B Antagonist Inhibits the Metastasis of Gastric Cancer Cells and Enhances the Efficacy of Cisplatin

Dihydroartemisinin inhibits EMT progression in medullary thyroid carcinoma through Hippo signaling pathway regulated by IL-6

Wnt signaling in liver regeneration, disease, and cancer

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