Synthesis of PJOV56, a new quinoxalinyl-hydrazone derivative able to induce autophagy and apoptosis in colorectal cancer cells, and related compounds

Maranhão, Sarah Sant’Anna; Moura, Andréa Felinto; Oliveira, Augusto César Aragão; Lima, Daisy Jereissati Barbosa; Barros-Nepomuceno, Francisco Washington Araújo; Paier, Carlos Roberto Koscky; Pinheiro, Alessandra C.; Nogueira, Thaís Cristina Mendonça; Souza, Marcus V. N. de; Pessoa, Cláudia

doi:10.1016/j.bmcl.2019.126851

Cited by 16 publications

(9 citation statements)

References 22 publications

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“…The interaction between autophagy and apoptosis in colorectal cancer is mainly regulated by related signal transduction pathways and factors [ [48] , [49] , [50] ] ( Fig. 2 ).…”

Section: The Main Regulatory Factors Of the Interaction Between Autopmentioning

confidence: 99%

“…At present, relevant literature has reported related factors are involved in regulating the interaction between autophagic and cell apoptosis in other tumors, such as Beclin-1, P62, caspase, Bcl-2 and so on [ 51 , 52 ]. It was also found that these related regulatory factors were involved in the interaction between autophagic and apoptosis in colorectal cancer [ 48 , 53 ] ( Fig. 2 ), the following key describes several major factors of interaction between autophagy and apoptosis: Fig.…”

Section: The Main Regulatory Factors Of the Interaction Between Autopmentioning

confidence: 99%

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The interaction mechanism between autophagy and apoptosis in colon cancer

Xie

Liu

2020

Translational Oncology

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Autophagy and apoptosis play crucial roles in tumorigenesis. Recent studies have shown that autophagy and apoptosis have a cross-talk relationship in anti-tumor therapy. It is well established that apoptosis is one of the main pathways of tumor cell death. While autophagy can occurs in tumors with opposite function: protective autophagy and lethal autophagy. Protective autophagy can inhibit tumor apoptosis induced by anticancer drugs, while lethal autophagy can induce tumor cell apoptosis in cooperation with anticancer drugs. Hence, autophagy and apoptosis have synergistic and antagonistic effects in tumor. Colorectal cancer is a common malignant tumor with high morbidity and mortality. In recent years, colorectal carcinoma has achieved improved clinical efficacy with drug treatment. Nonetheless, increasing drug-resistance limit the treatment efficacy, highlighting the urgency of exploring the molecular events that drive drug resistance. Researchers have found that autophagy is one of the major factors leading to drug resistance in colon cancer. Therefore, elucidating the interaction between autophagy and apoptosis is helpful to improve the efficacy of anticancer drugs in clinical treatment of colorectal cancer. This review attaches great importance to the relationship between autophagy and apoptosis and related factors in colorectal cancer.

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“…The interaction between autophagy and apoptosis in colorectal cancer is mainly regulated by related signal transduction pathways and factors [ [48] , [49] , [50] ] ( Fig. 2 ).…”

Section: The Main Regulatory Factors Of the Interaction Between Autopmentioning

confidence: 99%

Section: The Main Regulatory Factors Of the Interaction Between Autopmentioning

confidence: 99%

The interaction mechanism between autophagy and apoptosis in colon cancer

Xie

Liu

2020

Translational Oncology

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“…To further understand the role of DGKZ in CC progression, DEPs in SiHa cells with or without transfection of sh-DGKZ were enriched and analyzed by GO and KEGG biological analysis. GO analysis indicated that DEPs triggered by DGKZ depletion mostly induced macro-autophagy and macromitophagy, which regulated cell apoptosis and cell cycle in most cancer development [20][21][22]. In KEGG pathway analysis, the significant alteration was closely associated with autophagy or mitophagy including lysosome, phagosome and PI3K-Akt signaling pathway.…”

Section: Discussionmentioning

confidence: 95%

Downregulation of Diacylglycerol kinase zeta (DGKZ) suppresses tumorigenesis and progression of cervical cancer by facilitating cell apoptosis and cell cycle arrest

et al. 2021

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Diacylglycerol kinase zeta (DGKZ) participates in cancer progression. Here, the current work aims to identify the functional role of DGKZ in cervical cancer (CC). DGKZ expression in cervical cancer tissues and paired adjacent normal cervical tissues was assessed using Immunohistochemistry assay. SiHa and HeLa cells were transfected with lentivirus plasmids (sh-DGKZ or sh-NC) to evaluate the effects of DGKZ knockdown on cell proliferation, apoptosis and cell cycle distribution in vitro. Furthermore, BALB/c nude mice were injected subcutaneously with Lentivirus-sh-DGKZ-SiHa cells or Lentivirus-sh-NC-SiHa cells to analyze the influence of DGKZ silencing on tumor growth of CC in vivo. Moreover, the potential molecular mechanisms were predicted by GO and KEGG analysis and preliminarily explored through PathScan Analysis. Elevated DGKZ expression in cervical tumor was observed. Downregulation of DGKZ repressed proliferation and boosted apoptosis of SiHa and HeLa cells and induced cell cycle arrest at G0/G1 phase. In addition, Knockdown of DGKZ restrained tumor growth in tumor xenograft mice. Importantly, GO and KEGG analysis displayed that differentially expressed proteins induced by silence of DGKZ were mostly enriched in autophagy or mitophagy, indicating that the functions of DGKZ on cell proliferation and tumor growth may be associated with autophagy or mitophagy. PathScan analysis presented that PI3K-AKT and TAK1-NF-κB signaling pathways were prominently inhibited in SiHa cells transfected with sh-DGKZ. In summary, downregulation of DGKZ impeded cell proliferation, boosted cell apoptosis and induced cell cycle arrest to suppress tumorigenesis and progression of cervical cancer.

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“…It has been reported that the some chemotherapeutic drug-stimulated autophagy pathway can activate caspase-3, thereby inducing the apoptosis of tumor cells (Mowers et al, 2018). At same times, studies have confirmed that cell death in CRC can be achieved by inducing autophagy-dependent apoptosis pathways (Pedro et al, 2015;Grasso et al, 2016;Nagappan et al, 2017;Xia et al, 2017;Maranhão et al, 2020).…”

Section: Introductionmentioning

confidence: 91%

Cryptotanshinone Inhibits the Growth of HCT116 Colorectal Cancer Cells Through Endoplasmic Reticulum Stress-Mediated Autophagy

Zhao

et al. 2021

Front. Pharmacol.

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Among cancers, colorectal cancer (CRC) has one of the highest annual incidence and death rates. Considering severe adverse reactions associated with classical chemotherapy medications, traditional Chinese medicines have become potential drug candidates. In the current study, the effects of cryptotanshinone (CPT), a major component of Salvia miltiorrhiza Bunge (Danshen) on CRC and underlying mechanism were explored. First of all, data from in vitro experiments and in vivo zebrafish models indicated that CPT selectively inhibited the growth and proliferation of HCT116 and SW620 cells while had little effect on SW480 cells. Secondly, both ER stress and autophagy were associated with CRC viability regulation. Interestingly, ER stress inhibitor and autophagy inhibitor merely alleviated cytotoxic effects on HCT116 cells in response to CPT stimulation, while have little effect on SW620 cells. The significance of apoptosis, autophagy and ER stress were verified by clinical data from CRC patients. In summary, the current study has revealed the anti-cancer effects of CPT in CRC by activating autophagy signaling mediated by ER stress. CPT is a promising drug candidate for CRC treatment.

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Synthesis of PJOV56, a new quinoxalinyl-hydrazone derivative able to induce autophagy and apoptosis in colorectal cancer cells, and related compounds

Cited by 16 publications

References 22 publications

The interaction mechanism between autophagy and apoptosis in colon cancer

The interaction mechanism between autophagy and apoptosis in colon cancer

Downregulation of Diacylglycerol kinase zeta (DGKZ) suppresses tumorigenesis and progression of cervical cancer by facilitating cell apoptosis and cell cycle arrest

Cryptotanshinone Inhibits the Growth of HCT116 Colorectal Cancer Cells Through Endoplasmic Reticulum Stress-Mediated Autophagy

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