Effects of Lidocaine and Ropivacaine on Gastric Cancer Cells Through Down-regulation of ERK1/2 Phosphorylation <i>In Vitro</i>

Yang, Wenjing; Cai, Jun; Zhang, Huiming; Wang, Guyan; Jiang, Wen Guo

doi:10.21873/anticanres.13042

Cited by 24 publications

(26 citation statements)

References 21 publications

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“…Famous for cheapness and availability, local anesthetics are used extensively before operations in order to ease the pain (Yang et al, 2018). A large number of researches have demonstrated that local anesthetics can indirectly regulate the progression of various cancers.…”

Section: Discussionmentioning

confidence: 99%

“…Compelling evidence has indicated that Ropivacaine can induce apoptosis of hepatocellular carcinoma cells via activation of caspase-3 expression (Wang et al, 2019). Accumulating evidence has highlighted the importance of Ropivacaine in inhibition of cancers, such as breast cancer, colon cancers and gastric cancer (Castelli et al, (2020) ;Siekmann, Tina, von Sydow, & Gupta, 2019;Yang et al, 2018). However, the role of Ropivacaine in the progression of PTC has not been clearly probed.…”

Section: Introductionmentioning

confidence: 99%

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Ropivacaine inhibits proliferation, invasion, migration and promotes apoptosis of papillary thyroid cancer cells via regulating ITGA2 expression

Qin

Liu

Wang³

2020

Drug Development Research

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The present study aimed to investigate the roles of Ropivacaine in papillary thyroid cancer (PTC) and identify the possible mechanisms. The expression of integrin alpha‐2 (ITGA2) in TC cell lines was tested using Western blotting and RT‐qPCR. Subsequently, the level of ITGA2 in human PTC cell line (TPC‐1) was measured following intervention with a series of concentrations of Ropivacaine. Then, cell counting kit‐8 (CCK‐8) assay and colony formation assay were executed for detecting proliferation of cells after transfection with ITGA2 pcDNA3.1. The expression of proliferation‐related protein was determined by Western blotting. Additionally, the abilities of TPC‐1 cell invasion and migration were examined using Transwell assay and scratch wound healing assay. Apoptosis of TPC‐1 cells was analyzed using TUNEL assay and the expressions of apoptosis‐related proteins were tested via West blotting. The results suggested that ITGA2 was highly expressed in TC cell lines, especially in TPC‐1 cells. Ropivacaine decreased the expression of ITGA2 in a dose‐dependent manner. Moreover, after treatment with Ropivacaine, cell proliferation was inhibited accompanied by changes of proliferation‐related protein expressions, which was reversed following co‐transfection with ITGA2 pcDNA3.1. Furthermore, Ropivacaine concentration‐dependently suppressed invasion and migration of TPC‐1 cells, whereas these inhibitory effects were attenuated after ITGA2 overexpression. Furthermore, apoptosis was promoted, coupled with a decrease of Bcl‐2 expression and increases of Bax, cleaved caspase‐3 and cleaved caspase‐9 expression, in Ropivacaine‐treated TPC‐1 cells, which was restored following ITGA2 overexpression. These findings demonstrated that Ropivacaine could suppress proliferation, invasion, migration, and accelerate apoptosis of PTC cells via regulating ITGA2 expression.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Ropivacaine inhibits proliferation, invasion, migration and promotes apoptosis of papillary thyroid cancer cells via regulating ITGA2 expression

Qin

Liu

Wang³

2020

Drug Development Research

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“…Currently, growing researches have confirmed that lidocaine may perform anticancer effects on the therapy of diverse cancers through affecting tumor cell malignant behaviors, such as cell viability, apoptosis, migration and drug resistance. 4,8,21,22 In fact, sustaining proliferation and resisting apoptosis are two significant hallmarks of cancer cells that contribute to cancer cell malignant enlargement and progression, and proliferation inhibition and apoptosis promotion of cancer cells are promising methods to hinder the development of human cancers. 23 In this study, lidocaine up-regulated the proproliferative protein Cyclin D1 and pro-apoptotic proteins cleaved-Caspase-3 and cleaved-Caspase-9, which Figure 7 Lidocaine mediates CRC cell viability loss, apoptosis induction and aerobic glycolysis suppression by regulating miR-138-5p/HEY1 axis.…”

Section: Discussionmentioning

confidence: 99%

<p>Lidocaine Suppresses Cell Proliferation and Aerobic Glycolysis by Regulating circHOMER1/miR-138-5p/HEY1 Axis in Colorectal Cancer</p>

Zhang

et al. 2020

CMAR

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Background: Increasing evidence has uncovered the anticancer activity of lidocaine in many cancers. However, the role and the underlying molecular mechanism of lidocaine in colorectal cancer (CRC) remain poorly understood. Materials and Methods: Cell viability and apoptosis were measured by cell counting kit-8 assay and flow cytometry. Western blot was used to detect the protein of p53, CyclinD1, Procaspase-3, Cleaved-caspase-3, Pro-caspase-9, Cleaved-caspase-9, and hes-related family bHLH transcription factor with YRPW motif 1 (HEY1). Glycolytic metabolism was calculated by measuring the glucose consumption, lactate production and adenosine triphosphate (ATP) contents. The expression of circRNA homer scaffold protein 1 (circHOMER1), microRNA (miR)-138-5p and HEY1 mRNA was detected by quantitative real-time polymerase chain reaction. The interaction between miR-138-5p and circHOMER1 or HEY1 was analyzed using the dual-luciferase reporter assay. In vivo experiments were performed using the murine xenograft model. Results: Lidocaine suppressed CRC cell viability and aerobic glycolysis but promoted cell apoptosis in vitro as well as hindered tumor growth in vivo. CircHOMER1 was elevated in CRC tissues and cells, while lidocaine decreased circHOMER1 expression in CRC cells. Additionally, circHOMER1 overexpression reversed the anti-tumor activity of lidocaine in CRC cells. miR-138-5p was confirmed to interact with circHOMER1 and HEY1 in CRC cells directly, and circHOMER1 regulated HEY1 expression through repressing miR-138-5p expression. Besides, rescue assay indicated the anti-tumor activity mediated by lidocaine could be regulated by circHOMER1/miR-138-5p/HEY1 axis. Conclusion: Lidocaine mediated CRC cell viability loss, apoptosis induction and aerobic glycolysis inhibition by regulating circHOMER1/miR-138-5p/HEY1 axis, providing a novel treatment option for lidocaine to prevent the progression of CRC.

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“…On gastric cancer cells AGS and HGC-27 cells, lidocaine (10 μM) suppressed the proliferation and migration, while it exerted no invasion inhibitory effects on both cancer cells. ERK1/2, key kinases playing pivotal roles in speeding the gastric cancer cells proliferation ( Ahn et al, 2017 ), were down-regulated by lidocaine ( Yang W. et al, 2018 ). Interestingly, another local anesthetic, ropivacaine was also found to possess similar efficacy as lidocaine as shown in this study ( Yang W. et al, 2018 ).…”

Section: Lidocaine In Cancer Treatmentmentioning

confidence: 99%

Repositioning Lidocaine as an Anticancer Drug: The Role Beyond Anesthesia

Zhou

Wang

Cui

et al. 2020

Front. Cell Dev. Biol.

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While cancer treatment has improved dramatically, it has also encountered many critical challenges, such as disease recurrence, metastasis, and drug resistance, making new drugs with novel mechanisms an urgent clinical need. The term “drug repositioning,” also known as old drugs for new uses, has emerged as one practical strategy to develop new anticancer drugs. Anesthetics have been widely used in surgical procedures to reduce the excruciating pain. Lidocaine, one of the most-used local anesthetics in clinical settings, has been found to show multi-activities, including potential in cancer treatment. Growing evidence shows that lidocaine may not only work as a chemosensitizer that sensitizes other conventional chemotherapeutics to certain resistant cancer cells, but also could suppress cancer cells growth by single use at different doses or concentrations. Lidocaine could suppress cancer cell growth in vitro and in vivo via multiple mechanisms, such as regulating epigenetic changes and promoting pro-apoptosis pathways, as well as regulating ABC transporters, metastasis, and angiogenesis, etc., providing valuable information for its further application in cancer treatment and for new drug discovery. In addition, lidocaine is now under clinical trials to treat certain types of cancer. In the current review, we summarize the research and analyze the underlying mechanisms, and address key issues in this area.

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Effects of Lidocaine and Ropivacaine on Gastric Cancer Cells Through Down-regulation of ERK1/2 Phosphorylation In Vitro

Cited by 24 publications

References 21 publications

Ropivacaine inhibits proliferation, invasion, migration and promotes apoptosis of papillary thyroid cancer cells via regulating ITGA2 expression

Ropivacaine inhibits proliferation, invasion, migration and promotes apoptosis of papillary thyroid cancer cells via regulating ITGA2 expression

<p>Lidocaine Suppresses Cell Proliferation and Aerobic Glycolysis by Regulating circHOMER1/miR-138-5p/HEY1 Axis in Colorectal Cancer</p>

Repositioning Lidocaine as an Anticancer Drug: The Role Beyond Anesthesia

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