Effects of local anesthetics on cancer cells

Liu, Hengrui; Dilger, James P.; Lin, Jun

doi:10.1016/j.pharmthera.2020.107558

Cited by 80 publications

(59 citation statements)

References 86 publications

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“…To determined a proper concentration for this study, we rstly measured the IC 50 of carvacrol and cisplatin inhibition toward viability of ve TNBC cell lines we used in this study. Cell viability was determined using a common viability assay, MTT assay [41]. After 48 hours exposure, the IC 50 of carvacrol for all ve TNBC cell lines ranged from 193 − 166 µM.…”

Section: Ic50 Of Carvacrol and Cisplatin Inhibition Toward Viability mentioning

confidence: 99%

Carvacrol Promotes Cisplatin-induced Apoptosis of Triple-negative Breast Cancer Through TRPM7 Channels

Li¹,

Yé²,

Wang³

et al. 2021

Preprint

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Triple-negative breast cancer (TNBC) is the most dangerous type of breast cancer. Cisplatin is a chemotherapy agent for solid tumors treatments, but it is subjected to drug resistance. A natural compound, carvacrol, showed anti-cancer potential for TNBC and can be a cisplatin sensitizer. Carvacrol inhibits the transient receptor potential melastatin-like 7 channel (TRPM7), which plays a critical role in cancer apoptosis. In this study, we proposed that carvacrol can promote cisplatin-induced apoptosis of TNBC through TRPM7 channels. We tested this hypothesis using five TNBC cell lines. Cell viability and apoptosis were determined using the MTT and Bax (Bcl-2-associated X protein) ELISA respectively. 4T1 /BALB/c mice model was used to test the effect of carvacrol on cisplatin treatment. TRPM7 and Bax expression in the tumors were determined using western blotting. We also tested the effect of TRPM7 knockdown and TRPM7 inhibitor, 2-APB, on carvacrol actions in MDA-MB-231. The TRPM7 channel inhibition by carvacrol was confirmed using patch-clamp and Fura-2-based fluorescence quench assay. Results showed that carvacrol enhanced the suppression of cisplatin and cisplatin-induced apoptosis in all five TNBC cancer cell lines. Carvacrol improved cisplatin treatment in mice model by promoting cisplatin-induced apoptosis in tumors, but did not affect TRPM7 in tumors. Both knockdown and 2-APB inhibition of TRPM7 channels eliminated the effects of carvacrol and 2-APB showed a similar effect as carvacrol. Our study demonstrated that carvacrol is a cisplatin sensitizer in TNBC chemotherapy and TRPM7 channels might play a role in the synergistic effect of carvacrol on cisplatin.

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Section: Ic50 Of Carvacrol and Cisplatin Inhibition Toward Viability mentioning

confidence: 99%

Carvacrol Promotes Cisplatin-induced Apoptosis of Triple-negative Breast Cancer Through TRPM7 Channels

Li¹,

Yé²,

Wang³

et al. 2021

Preprint

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“…The MTT assay was rst reported by Mossmann in 1983 [38]. It is commonly used for both cancer cell and non-cancer cell viability determination [39,40]. Brie y, cells were grown in 96 well plates and at the endpoint of the culture time, the culture medium was removed and 0.8 mg/ml of MTT working solution (dissolved in serum-free medium) was added to the wells.…”

Section: Mtt Assaymentioning

confidence: 99%

LncRNA STK4 antisense RNA 1(STK4-AS1) affects the osteosarcoma cell cycle by regulating p53 protein

Yao

Hou

Liu

et al. 2021

Preprint

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Background: LncRNA STK4-AS1 has been identified as a potential biomarker associated with multiple cancers. We proposed that STK4-AS1 plays a role in the proliferation of osteosarcoma by regulating its cell cycle. Methods: We compared the expression of STK4-AS1 in osteosarcoma vs normal samples both in clinical tissues and cell lines. We overexpressed and knockdown STK4-AS1 in p53 expressing osteosarcoma cells U2OS and p53 muted expressing osteosarcoma cells MG63 and analyzed cell viability and cell cycle. We overexpressed p53 in STK4-AS1 knockdown cells to explore the association of STK4-AS1 and p53 in the cell cycle. Results: The STK4-AS1 expression was higher in osteosarcoma tissue than adjacent normal bone tissues and was higher in osteosarcoma cell lines (U2OS, MG63, and SAOS-2) than in osteoblast cell lines (hFOB and HOB). Knockdown of STK4-AS1 in U2OS decreased the cell viability, increased cells in the G0/G1 phase, decreased cells in the S and G2/M phase, decreased expression of cyclin A and B, increased p53 and p21, and had no effect on cyclin D and cyclin E, while overexpression did the opposes. MG63 cell viability was not affected by altered STK4-AS1 levels. P53 overexpression in STK4-AS1 knockdown cells recovered cell viability, p21, cyclin A, and cyclin B expression. Conclusion: LncRNA STK4-AS1 affected p53 expressing osteosarcoma cells U2OS cell viability through regulating cell cycle, which is mediated by p53/p21 pathway.

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“…82 Tumor cell membranes have VGSCs, which are associated with tumor cell invasion and metastasis. [83][84][85] There have been recent studies carried out on the antitumor properties of local anesthetics (Table 3). Sakaguchi et al reported that clinical lidocaine concentration inhibited the proliferation of the human tongue cancer cell line CAL27 induced by serum and epidermal growth factor.…”

Section: Local Anesthetic Agentsmentioning

confidence: 99%

<p>Effects of Anesthesia on Postoperative Recurrence and Metastasis of Malignant Tumors</p>

Fan¹,

Wang²,

Chen³

et al. 2020

CMAR

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It is difficult to control the recurrence and metastasis of malignant tumors; furthermore, anesthesia is considered one of the main influencing factors. There has been increasing clinical attention on the effects of anesthetic drugs and methods on postoperative tumor growth and metastasis. We reviewed the effects of anesthesia on tumor recurrence and metastasis; specifically, the effects of anesthetic agents, anesthesia methods, and related factors during the perioperative period on the tumor growth and metastasis were analyzed. This study can provide reference standards for rational anesthesia formulations and cancerrelated pain analgesia protocols for surgical procedures in patients with malignant tumors. Moreover, it contributes toward an experimental basis for the improvement and development of novel anesthetic agents and methods.

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Effects of local anesthetics on cancer cells

Cited by 80 publications

References 86 publications

Carvacrol Promotes Cisplatin-induced Apoptosis of Triple-negative Breast Cancer Through TRPM7 Channels

Carvacrol Promotes Cisplatin-induced Apoptosis of Triple-negative Breast Cancer Through TRPM7 Channels

LncRNA STK4 antisense RNA 1(STK4-AS1) affects the osteosarcoma cell cycle by regulating p53 protein

<p>Effects of Anesthesia on Postoperative Recurrence and Metastasis of Malignant Tumors</p>

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