&lt;p&gt;Knockdown of ROS proto-oncogene 1 inhibits migration and invasion in gastric cancer cells by targeting the PI3K/Akt signaling pathway&lt;/p&gt;

Jian, Qiao; Li, Man; Sun, Dan; Li, Wenhui

doi:10.2147/ott.s213421

Cited by 4 publications

(4 citation statements)

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“…39 And it is also found that the migration and invasion of GC cells are attenuated by inhibiting the PI3K/AKT signaling pathway. 40 In addition, PI3K/AKT signaling pathway can also affect EMT. For example, breast cancer 1 (AIB1) enhances EMT by activating PI3K/AKT signaling.…”

Section: Discussionmentioning

confidence: 99%

<p>Ropivacaine Inhibits the Growth, Migration and Invasion of Gastric Cancer Through Attenuation of WEE1 and PI3K/AKT Signaling via miR-520a-3p</p>

Zhang¹,

Xing²,

Gu³

et al. 2020

OTT

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Background: Metastasis remains one of the greatest challenges involved in treating gastric cancer (GC). Ropivacaine (Rop) is not only a well-documented local anesthetic medicament but also has been reported to exert an antitumor role in cancer development. This study explored the effects of ropivacaine on the growth, migration and invasion of gastric cancer and the underlying mechanisms. Methods: Cell Counting Kit-8 (CCK8) assay was conducted to test the effect of Rop on the proliferation of AGS and BGC-823 GC cells. Moreover, cell apoptosis, migration and invasion were examined by flow cytometry and transwell assay, respectively. The expression of miR-520a-3p was determined by qRT-PCR. miRNA targeting sites were analyzed using bioinformatics analysis and dual-luciferase reporter assay. Protein levels of WEE1 and PI3K/ AKT were detected by Western blot. Furthermore, the tumor-forming experiment of nude mice was used to detect the growth of cells in vivo. Results: Rop inhibited proliferation but promoted apoptosis of GC cells. Besides, the migration and invasion of GC cells were also inhibited by Rop. Moreover, miR-520a-3p expression was enhanced by Rop, and transfection with miR-520a-3p mimic decreased cell proliferation, migration and invasion. The upregulation of miR-520a-3p was partly contributed to the inhibitory effect of ropivacaine on GC cell lines. Finally, Rop inactivated WEE1 and PI3K/AKT pathway via upregulation of miR-520a-3p. Conclusion: Our results suggested that Rop decreased growth, migration and invasion of GC cells via regulating miR-520a-3p expression and further inactivated WEE1 and PI3K/ AKT signaling pathways.

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Section: Discussionmentioning

confidence: 99%

<p>Ropivacaine Inhibits the Growth, Migration and Invasion of Gastric Cancer Through Attenuation of WEE1 and PI3K/AKT Signaling via miR-520a-3p</p>

Zhang¹,

Xing²,

Gu³

et al. 2020

OTT

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“…Moreover, the numbers of invaded cells decreased after treatment with ethyl acetate extract of H. hirsute in dose dependent manner. Metastasis is a complex process, which is related to multiple intracellular signals such as production of reactive oxygen species (ROS) [29,30], and contribution of microRNAs (miRNAs) [31,32]. These changes elevate EMT, leading to increases in migration and invasion of cancer cells [33,34].…”

Section: Discussionmentioning

confidence: 99%

Ethyl Acetate Extract of Helicteres hirsuta Suppresses MCF-7 Human Breast Cancer Cell Mobility

Nguyen

Thi

Tường

et al. 2022

ARRB

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Objective: To investigate the anticancer activity of Helicteres hirsuta (H. hirsute) extract against a breast cancer cell line- MCF7. Methods: H. hirsute was extracted in absolute methanol. Further, the crude extract was further partitioned in n-hexane, chloroform and ethyl acetate. The total phenolic and flavonoid content were determined by using spectroscopic methods with gallic acid and quercetin standard compounds, respectively. Anticancer activities of H. hirsuta extract was elucidated by MTT, wound headling, and transwell invasion assays. Results: Total phenolic compounds in H. hirsute extracts reached 22.07 ± 2.54, 58.57 5.54 and 235.56 ± 7.54 mg GAE/g in each n hexan, chloroform, ethyl acetate fractions, respectively. Whereas the ethyl acetate fraction showed the greatest phenolic contents with 235.56 ± 7.54 mg GAE/g. Moreover, the flavonoid contents of H. hirsute extracts reached 5.76 ± 0.94, 9.25 ± 1.84 and 19.37 ± 2.57 mg quercetin equivalent/g in each n hexan, chloroform, ethyl acetate fractions, respectively, in which, the ethyl acetate fraction also showed the highest amounts of flavonoid contents. Further, the ethyl acetate of H. hirsute significantly decreased the viability of breast cancer MCF7 cells after 48 h treatment with IC50 value of 95 ± 2.54 \(\mu g/mL\) compared to control. In addition, the ethyl acetate extract of H. hirsute suppressed the invasion and migration of MCF7 cell lines in a dose-dependent manner at non-toxic concentrations. Conclusions: The ethyl acetate of H. hirsute suppressed the growth and motility of breast cancer MCF7 cells.

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“…The function of the PI3K/AKT signaling pathway is significantly correlated with the BAG4-induced EMT and the expression of ZEB1 [ 61 ]. Meanwhile, silencing ROS1 , an oncogene that encodes a tyrosine kinase of the insulin receptor family, attenuated GC cell invasion and EMT through the PI3K/Akt signaling pathway [ 62 ]. Carcinoembryonic antigen-related cell adhesion molecule 6 (CEACAM6), a glycosylphosphatidylinositol-linked immunoglobulin superfamily member, has pivotal oncogenic roles by inducing EMT as validated by upregulations in the EMT markers N-cadherin, Vimentin, and Slug.…”

Section: Signaling Pathways Involved In Gc Invasion and Metastasismentioning

confidence: 99%

Molecular Insight into Gastric Cancer Invasion—Current Status and Future Directions

Matsuoka,

Yashiro

2023

Cancers

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Gastric cancer (GC) is one of the most common malignancies worldwide. There has been no efficient therapy for stage IV GC patients due to this disease’s heterogeneity and dissemination ability. Despite the rapid advancement of molecular targeted therapies, such as HER2 and immune checkpoint inhibitors, survival of GC patients is still unsatisfactory because the understanding of the mechanism of GC progression is still incomplete. Invasion is the most important feature of GC metastasis, which causes poor mortality in patients. Recently, genomic research has critically deepened our knowledge of which gene products are dysregulated in invasive GC. Furthermore, the study of the interaction of GC cells with the tumor microenvironment has emerged as a principal subject in driving invasion and metastasis. These results are expected to provide a profound knowledge of how biological molecules are implicated in GC development. This review summarizes the advances in our current understanding of the molecular mechanism of GC invasion. We also highlight the future directions of the invasion therapeutics of GC. Compared to conventional therapy using protease or molecular inhibitors alone, multi-therapy targeting invasion plasticity may seem to be an assuring direction for the progression of novel strategies.

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<p>Knockdown of ROS proto-oncogene 1 inhibits migration and invasion in gastric cancer cells by targeting the PI3K/Akt signaling pathway</p>

Cited by 4 publications

References 44 publications

<p>Ropivacaine Inhibits the Growth, Migration and Invasion of Gastric Cancer Through Attenuation of WEE1 and PI3K/AKT Signaling via miR-520a-3p</p>

<p>Ropivacaine Inhibits the Growth, Migration and Invasion of Gastric Cancer Through Attenuation of WEE1 and PI3K/AKT Signaling via miR-520a-3p</p>

Ethyl Acetate Extract of Helicteres hirsuta Suppresses MCF-7 Human Breast Cancer Cell Mobility

Molecular Insight into Gastric Cancer Invasion—Current Status and Future Directions

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