Illustrations
Figure 1
Cell viability assessed by MTT assay in experimental groups at 24, 48 and 72 h of treatment (n=6, each group). The viability decreased in ALA-PDT treatment group at 24, 48 and 72 h. *p<0.05 vs. control group at an identical time point. Treatments with ERK1/2, P38 and JNK inhibitors further decreased the cell viability, ** p<0.01 vs. control group, except the P38 inhibitor groups at 48h.
Figure 1
Figure 2
Cell death detected by annexin-V and propidium iodide (PI) in experimental groups. A-G) flow cytometry results showing the percent of annexin-V positive and PI positive cells after 72 h of treatment. H) bar graph summarizes the percentage of annexin-V positive and PI positive cells at 24, 48 and 72 h after treatment. ** p<0.01 vs. control group and #p<0.05 vs. ALA-PDT group. *p<0.05 vs. control group and ** p<0.01 vs. control group.
Figure 2
Figure 3
Ultrastructural alterations in the experimental groups after 72 h of treatment. Compared to control, ALA-PDT resulted in necrocytosis, apoptotic bodies, karyopyknosis, karyorrhexis, and reduced numbers of organelles at 72 h. In the ERK1/2 inhibitor treatment group there were almost no organelles within the cytoplasm, the chromatin had dissolved and microvilli were absent.
Figure 3
Figure 4
Immunocytochemistry showing the staining of p-MEK, p-ERK1/2 and p-ELK-1 in SCL-1 cells in the experimental groups. Very low background staining of p-MEK, p-ERK1/2 and p-ELK-1 were observed in the control, ALA and light treatment groups at 60 min. The fluorescent signals were significantly enhanced by ALA-PDT treatment. Inhibition of ERK1/2 reduced the fluorescent intensities of the detected proteins back to levels comparable with controls.
Figure 4
Figure 5
Protein levels of total and phosphorylated MEK, ERK1/2, and Elk-1 under various conditions at 30, 60 and 90 min after treatment. ALA-PDT increased and ERK1/2 inhibitor suppressed p-MEK, p-ERK1/2 and p-Elk-1 levels. A, Representative Western Blots. GAPDH was used as an internal protein loading control; B, Summarized band intensity for p-MEK; C, Summarized band intensity for p-ERK1/2; D, summarized band intensity for p-Elk-1. Data were presented as means+/- S.E. *p<0.01 vs. other groups.
Figure 5
Figure 6
Protein levels of total and phosphorylated p38 and Elk-1 under various experimental conditions after 30-90 min treatments. A) Representative Western Blots. B) Summarized band intensity for p-p38; C, Summarized band intensity for p-Elk-1. Data were presented as means +/- S.E. *p<0.001 vs. other groups.
Figure 6
Figure 7
Protein levels of phosphorylated JNK, c-Jun and Elk-1 under experimental conditions after 30-90 min treatments. A) Representative Western Blots. B) Summarized band intensity for p-JNK; C) Summarized band intensity for p-c-JUN and p-Elk-1. Data were presented as means+/- S.E. *p<0.001 vs. other groups.
Figure 7
Auteurs
1 Institute for Cancer Research,
School of Basic Medical Science,
Health science center of Xi’an Jiaotong University,
Xi’an,
P. R. China
2 Department of Dermatology,
3 Center of Laboratory Medicine,
General Hospital of Ningxia Medical University,
Yinchuan,
P. R. China
4 Department of Pathology,
Basic Medical School,
Ningxia Medical University,
Yinchuan,
P. R. China
5 Department of Pharmaceutical Sciences,
North Carolina Central University,
Durham,
NC,
USA
6 Department of Dermatology,
People's Hospital of Zhangdian District,
Zibo City,
Shandong province,
P. R. China
The incidence of skin cancer has increased worldwide [1, 2]. Finding an effective treatment for SCC is therefore of great clinical significance. Over the last thirty years, a procedure known as photodynamic therapy (PDT) has been developed and is showing some success in combating SCC [3]. PDT employs the use of a drug, the photosensitizer or photosensitizing agent, which is taken up by the patient's cells. The photosensitizer tends to accumulate and be retained longer in cancerous cells than in normal [...]