Blocking the Glycolytic Pathway Sensitizes Breast Cancer to Sonodynamic Therapy

Xie, Linfeng; Feng, Xiaolan; Shi, Yin; He, Meng Xiao; Wang, Pan; Wang, Xiaobing; Mi, Zeyuan; Liu, Quanhong

doi:10.1016/j.ultrasmedbio.2018.01.020

Cited by 14 publications

(7 citation statements)

References 34 publications

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“…Besides, SDT increases the sensitivity of tumor cells to 2DG treatment by blocking the energy replenishment pathways. Ultimately, the tumor inhibition rate of the combined therapy was higher than the monotherapies (Xie et al, 2018). The findings indicate that SDT +2DG could provide a new noninvasive treatment for high mortality metastatic tumors.…”

Section: The Glycolysis Blockage Aggravated Sdt Effectsmentioning

confidence: 88%

The Application of DVDMS as a Sensitizing Agent for Sono-/Photo-Therapy

Mai¹,

Wang²,

Liu³

et al. 2020

Front. Pharmacol.

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Both photodynamic therapy (PDT) and sonodynamic therapy (SDT) are fast growing activated therapies by using light or ultrasound to initiate catalytic reaction of sensitizing agents, showing great potentials in clinics because of high safety and noninvasiveness. Sensitizers are critical components in PDT and SDT. Sinoporphyrin sodium (DVDMS) is an effective constituent derived from Photofrin that has been approved by FDA. This review is based on previous articles that explore the applications of DVDMS mediated photodynamic/sonodynamic cancer therapy and antimicrobial chemotherapy. Researchers utilize different cell lines, distinct treatment protocols to explore the enhanced therapeutic response of neoplastic lesion. Moreover, by designing a series of nanoparticles for loading DVDMS to improve the cellular uptake and antitumor efficacy of PDT/SDT, which integrates diagnostics into therapeutics for precision medical applications. During the sono-/photo-activated process, the balance between oxidation and antioxidation, numerous signal transduction and cell death pathways are also involved. In addition, DVDMS mediated photodynamic antimicrobial chemotherapy (PACT) can effectively suppress bacteria and multidrug resistant bacteria proliferation, promote the healing of wounds in burn infection. In brief, these efficient preclinical studies indicate a good promise for DVDMS application in the activated sono-/photo-therapy.

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Section: The Glycolysis Blockage Aggravated Sdt Effectsmentioning

confidence: 88%

The Application of DVDMS as a Sensitizing Agent for Sono-/Photo-Therapy

Mai¹,

Wang²,

Liu³

et al. 2020

Front. Pharmacol.

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“…Similar to PDT, DVDMS-SDT significantly inhibited PCNA levels and induced MMP loss [14,15,31,32,34,40]. ROS-induced mitochondrial-dependent apoptosis was the primary mechanism of cell killing by DVDMS-mediated SDT [34,[37][38][39], as evidenced by the upregulation of cleaved-caspase-3, -8, and -9, caspase-10, p-p38, p53, and Bax, the downregulation of Bcl-2 and RIPI3, and the release of cytochrome c (CytoC) [14,29,39,40]. DVDMS-SDT-induced ROS also led to a G2/M phase cell cycle arrest, decreased CDK1 and Cyclin B1 protein levels, and increased levels of the CDK inhibitors p21 and p27 [39].…”

Section: Antitumor Effects Of Dvdmsmediated Pdtmentioning

confidence: 91%

“…Li et al [34] investigated the feasibility of using DVDMS loaded into liposome-microbubble complexes (DLMBs) with SDT against breast cancer. Xie et al [14] found that 2-deoxyglucose (2DG), an antiglycolytic agent, enhanced the cytotoxicity and ROS generation of DVDMS-SDT. Sun et al [35] reported that ultrasound-targeted microbubble destruction (UTMD) and internalizing RGD (iRGD)-modified DVDMS liposomes (iRGD-Lipo-DVDMS) augmented the efficacy of SDT.…”

Section: Antitumor Effects Of Dvdmsmediated Pdtmentioning

confidence: 99%

“…Soon after, the antitumor effects of DVDMS-PDT and safety evaluations were completed, the efficacy of monomeric DVDMS was 10-fold stronger compared with Photofrin, and the toxicity was only increased by 2-fold, so the therapeutic window was greatly increased [9][10][11][12]. Interestingly, DVDMS was subsequently found to be activated by ultrasound and its antitumor effects via sonodynamic therapy (SDT) were demonstrated [13][14][15]. On October 31, 2013, Qinglong Hi-Tech Co., Ltd. submitted applications to the China Food and Drug Administration (CFDA) to register DVDMS as a photosensitizer, sonosensitizer, and radiotherapy sensitizer (Nos.…”

Section: Introductionmentioning

confidence: 99%

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Sinoporphyrin sodium, a novel sensitizer for photodynamic and sonodynamic therapy

Liu

et al. 2020

Open Chemistry

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AbstractSinoporphyrin sodium (DVDMS) is a novel sensitizer discovered by Professor Fang Qi-Cheng and widely used in photodynamic (PDT) and sonodynamic therapy (SDT). We searched databases including PubMed, Web of Science, CNKI, etc. for system review of its progress. We found that, both DVDMS-PDT and -SDT had been proven effective for inhibiting tumor growth and mechanisms involved reactive oxygen species, autophagy, and mitochondrial apoptosis pathways. Material advances enhanced antitumor effects and expanded its application. The safety of DVDMS in animals was evaluated, and metabolic parameters were uncovered. Additionally, DVDMS-PDT also exhibited therapeutic effects on non-neoplastic diseases like psoriasis and bacterial infections. Two phase I clinical trials of DVDMS have been documented, but recruitments had still not been completed. In conclusion, DVDMS is a promising sensitizer for both PDT and SDT; however, there are some shortcomings in previous studies like inconsistent treatment parameters, which need systematic assessments in future. Moreover, more mechanisms such as the role of autophagy need to be discovered. Further evidence of the safety and effectiveness of new materials are needed, and the application in non-neoplastic diseases like actinic keratosis and fungal infection deserves further development. Above all, promoting its clinical applications is the most important goal.

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“… 3 In recent years, much research on the treatment of malignant cancer has focused on glucose deprivation and/or blocking the glycolytic pathway. 4 , 5 Some research has shown that, under conditions of glucose deprivation, cells can be induced to apoptosis by the regulation of Bcl-2 family proteins through the following pathways: 1) glycogen synthase kinase 3β phosphorylates Mcl-1 (antiapoptotic Bcl-2 family protein with BH1-4 domain) and targets Mcl-1 for proteasome-mediated degradation 6 and 2) AMP-activated protein kinase (AMPK) is activated, induces the transcription of Bim (apoptotic Bcl-2 family protein with BH1-3 domain), and inactivates AMPK-dependent mammalian target of rapamycin, which can inhibit Mcl-1 transcription. 7 Other research has shown that glucose metabolism participates in apoptotic regulation by Bcl-2 family proteins.…”

Section: Introductionmentioning

confidence: 99%

Glucose deprivation promotes apoptotic response to S1 by enhancing autophagy in human cervical cancer cells

Zhou

Kong

Zhang

et al. 2018

CMAR

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BackgroundS1 is a novel BH3 mimetic that can induce death in some types of cancer cells, such as melanoma B16, ovarian cancer SKOV3, and U251 glioma cells. S1 inhibits Bcl-2 and Mcl-1 expression and induces cancer cell apoptosis. Cancer cell survival is highly dependent on glucose. Here, we observed the effect of glucose deprivation on the apoptotic response to S1 in human cervical cancer (HeLa) cells.Materials and methodsEarle’s balanced salt solution (EBSS) was used to simulate glucose deprivation. MTT assay was used to analyze the cell survival rate, and Hoechst 33342 dye was used to detect the apoptosis in HeLa cells. Western blotting was used to detect the expression of ER stress and autophagy relative proteins. In addition, lysosomes were observed with Lyso-Tracker staining by confocal microscopy.ResultsS1 decreased cell distribution density and survival rate, and MTT assay showed that EBSS enhanced the inhibitory effects of S1 on HeLa cell growth. Hoechst 33342 dye showed that S1 led to pyknosis, fragmentation, and strong staining in HeLa cell nuclei, and EBSS enhanced these effects. Western blotting indicated that EBSS enhanced the expression of apoptosis-related proteins (cytochrome C, caspase-3, and poly[ADP-ribose] polymerase 1) induced by S1 in HeLa cells. S1 decreased p62 expression and increased the autophagosome-associated protein LC3-II expression, which indicated that S1 induced autophagy in HeLa cells. EBSS enhanced S1-induced autophagy in HeLa cells. Furthermore, autophagy inhibitor chloroquine enhanced S1-induced apoptosis in HeLa cells.ConclusionThese results indicate that EBSS exacerbates S1-induced autophagy and severe autophagy induced by EBSS and S1 could lead to apoptosis in HeLa cells. The results also suggest that EBSS enhances the sensitivity of HeLa cells to S1-induced apoptosis and that autophagy plays an important role in this process.

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Blocking the Glycolytic Pathway Sensitizes Breast Cancer to Sonodynamic Therapy

Cited by 14 publications

References 34 publications

The Application of DVDMS as a Sensitizing Agent for Sono-/Photo-Therapy

The Application of DVDMS as a Sensitizing Agent for Sono-/Photo-Therapy

Sinoporphyrin sodium, a novel sensitizer for photodynamic and sonodynamic therapy

Glucose deprivation promotes apoptotic response to S1 by enhancing autophagy in human cervical cancer cells

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