Photodynamic therapy with the novel photosensitizer chlorophyllin f induces apoptosis and autophagy in human bladder cancer cells

Du, Lihuan; Zheng, Jiawei; Jiang, Ning; Wang, Guozeng; Yi-wei, Chu; Wei, Lin; Qian, Ji; Chen, Gang

doi:10.1002/lsm.22225

Cited by 23 publications

(15 citation statements)

References 37 publications

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“…This result suggests, first, that Beclin‐1 was not photodamaged, in agreement with other studies . Secondly, Beclin‐1 does not seem to participate in the autophagy induction after DMMB/light treatment, since other studies have reported increase in Beclin‐1 levels in parallel to autophagy induction . Thirdly, this result reinforces the argument that DMMB/light treatment causes mainly blockage of autophagic flux and that p53 plays no role in the consequent cell death.…”

Section: Discussionsupporting

confidence: 91%

p53‐Dependent and p53‐Independent Responses of Cells Challenged by Photosensitization

Abrantes

Dias

Souza-Pinto

et al. 2018

Photochem & Photobiology

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The p53 protein exerts fundamental roles in cell responses to a variety of stress stimuli. It has clear roles in controlling cell cycle, triggering apoptosis, activating autophagy and modulating DNA damage response. Little is known about the role of p53 in autophagy‐associated cell death, which can be induced by photoactivation of photosensitizers within cells. The photosensitizer 1,9‐dimethyl methylene blue (DMMB) within nanomolar concentration regimes has specific intracellular targets (mitochondria and lysosomes), photoinducing a typical scenario of cell death with autophagy. Importantly, in consequence of its subcellular localization, photoactive DMMB induces selective damage to mitochondrial DNA, saving nuclear DNA. By challenging cells having different p53 protein levels, we investigated whether p53 modulates DMMB/light‐induced phototoxicity and cell cycle dynamics. Cells lacking p53 activity were slightly more resistant to photoactivated DMMB, which was correlated with a smaller sub‐G1 population, indicative of a lower level of apoptosis. DMMB photosensitization seems to induce mostly autophagy‐associated cell death and S‐phase cell cycle arrest with replication stress. Remarkably, these responses were independent on the p53 status, indicating that p53 is not involved in either process. Despite describing some p53‐related responses in cells challenged by photosensitization, our results also provide novel information on the consequences of DMMB phototoxicity.

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Section: Discussionsupporting

confidence: 91%

p53‐Dependent and p53‐Independent Responses of Cells Challenged by Photosensitization

Abrantes

Dias

Souza-Pinto

et al. 2018

Photochem & Photobiology

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“…We then quantified autophagic activity by flow cytometry using the Cyto-ID assay, which fluorescently tags autophagosomes [26]. A 1.8-fold increase in mean fluorescence intensity was detected in ATRA treated NB4 cells at day 3 (Figure 1C).…”

Section: Resultsmentioning

confidence: 99%

Induction of autophagy is a key component of all-trans-retinoic acid-induced differentiation in leukemia cells and a potential target for pharmacologic modulation

Orfali

O’Donovan

Nyhan

et al. 2015

Experimental Hematology

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Acute myeloid leukemia (AML) is characterized by the accumulation of immature blood cell precursors in the bone marrow. Pharmacologically overcoming the differentiation block in this condition is an attractive therapeutic avenue, which has only achieved success in a subtype of AML, acute promyelocytic leukemia (APL). Attempts to emulate this success in other AML subtypes have thus far been unsuccessful. Autophagy is a conserved protein degradation pathway with important roles in mammalian cell differentiation, particularly within the hematopoietic system. In this study we demonstrate the functional importance of autophagy in APL cell differentiation. We show that autophagy is increased during ATRA-induced granulocytic differentiation of the APL cell line NB4, and that this is associated with increased expression of LC3-II and GATE-16 proteins involved in autophagosome formation. Autophagy inhibition, using either drugs (chloroquine/3-methyladenine) or short-hairpin (sh)RNA targeting the essential autophagy gene ATG7, attenuates myeloid differentiation. Importantly, we show that enhancing autophagy promotes ATRA-induced granulocytic differentiation of an ATRA-resistant derivative of the non-APL AML HL60 cell line (HL60-Diff-R). These data support the development of strategies to stimulate autophagy as a novel approach to promote differentiation in AML.

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“…Prior to the presentation of autophagy, LC3 generated in cells is modified and processed to become the regularly expressed, soluble type-I LC3 in the cytoplasm (28). When autophagy occurs, type-I LC3 is modified and processed via ubiquitin-type processing (29). Type-I LC3 forms type-II LC3 by combining with phosphatidyl ethanolamine on the surface of an autophagic membrane; type-II LC3 is always combined on the membrane of intracellular autophagic vacuoles (29).…”

Section: Discussionmentioning

confidence: 99%

Anticancer effect of salidroside reduces viability through autophagy/PI3K/Akt and MMP‑9 signaling pathways in human bladder cancer cells

Tian

Xu²,

Liu

2018

Oncol Lett

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Salidroside has a wide range of pharmacological activities, including antitumor, anti-inflammatory, analgesic, antibacterial, antiviral and anti-fertility abilities. In the present study, the effects of salidroside on the viability and apoptosis of bladder cancer cells, and the potential underlying mechanisms, were examined. In the present study, treatment with salidroside reduced cell viability, and induced apoptosis and caspase-9/3 activation in the T24 human bladder carcinoma cell line. Salidroside induced autophagy, promoted the protein expression of nucleoporin p62 and the microtubule-associated proteins 1A/1B light chain 3B, suppressed phosphoinositide 3-kinase (PI3K) and phosphorylated protein kinase B (p-Akt) expression, inhibited matrix metalloproteinase-9 (MMP-9) expression and increased that of Bcl-2-associated X protein, which functions as an apoptosis regulator in T24 cells. In the present study, it was demonstrated that the effect of salidroside reduced the viability and induced the apoptosis of bladder cancer cells through the autophagy/PI3K/Akt and MMP-9 signaling pathways.

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Photodynamic therapy with the novel photosensitizer chlorophyllin f induces apoptosis and autophagy in human bladder cancer cells

Cited by 23 publications

References 37 publications

p53‐Dependent and p53‐Independent Responses of Cells Challenged by Photosensitization

p53‐Dependent and p53‐Independent Responses of Cells Challenged by Photosensitization

Induction of autophagy is a key component of all-trans-retinoic acid-induced differentiation in leukemia cells and a potential target for pharmacologic modulation

Anticancer effect of salidroside reduces viability through autophagy/PI3K/Akt and MMP‑9 signaling pathways in human bladder cancer cells

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