Hedgehog (Hh) signaling pathway plays an essential role during vertebrate embryonic development and tumorigenesis. It is already known that Sonic hedgehog (Shh) pathway is important for the evolution of radio and chemo-resistance of several types of tumors. Most of the brain tumors are resistant to chemotherapeutic drugs, consequently, they have a poor prognosis. So, a better knowledge of the Shh pathway opens an opportunity for targeted therapies against brain tumors considering a multi-factorial molecular overview. Therefore, emerging studies are being conducted in order to find new inhibitors for Shh signaling pathway, which could be safely used in clinical trials. Shh can signal through a canonical and non-canonical way, and it also has important points of interaction with other pathways during brain tumorigenesis. So, a better knowledge of Shh signaling pathway opens an avenue of possibilities for the treatment of not only for brain tumors but also for other types of cancers. In this review, we will also highlight some clinical trials that use the Shh pathway as a target for treating brain cancer.

/pdf/a-highlight-on-sonic-hedgehog-pathway-2el1vsrs99.pdf

A highlight on Sonic hedgehog pathway

Stereotactic ablative radiotherapy for colorectal cancer liver metastasis.

Tunneling nanotubes mediate adaptation of Glioblastoma Cells to temozolomide and ionizing radiation treatment

Autophagy induced by ionizing radiation promotes cell death over survival in human colorectal cancer cells.

Alzheimer's disease (AD) is a common neurodegenerative disease in the elderly population. Autophagy is a well‑known regulator of neurodegenerative diseases and β‑asarone has been discovered to have certain neuropharmacological effects. Thus, the present study aimed to analyze the potential effects of β‑asarone in AD and its possible mechanism of action in relation to autophagy. The present study investigated the effects of β‑asarone on the number of senile plaques and amyloid β(Aβ)40, Aβ42, amyloid precursor protein (APP) and Beclin‑1 mRNA levels in the hippocampus of APP/presenilin‑1 (PS1) transgenic mice. The possible mechanism of β‑asarone on autophagy‑related proteins, including Beclin‑1, light chain (LC)3A, LC3B and p62 levels, and the number of autophagosomes was also investigated. Mice were divided into a normal control group, a model group, a β‑asarone‑treated group, a 3‑MA‑treated group and a rapamycin‑treated group. Treatments were continuously administered to all mice for 30 days by intragastric administration. The mice, including those in the normal and model control groups, were given equal volumes of saline. It was demonstrated that β‑asarone treatment reduced the number of senile plaques and autophagosomes, and decreased Aβ40, Aβ42, APP and Beclin‑1 expression in the hippocampus of model mice compared with untreated model mice. β‑asarone also inhibited LC3A/B expression levels, but increased p62 expression. It was deduced that the neuroprotective effects of β‑asarone in APP/PS1 transgenic mice resulted from its inhibition of autophagy. In conclusion, the data suggested that β‑asarone should be explored further as a potential therapeutic agent in AD.

/pdf/b-asarone-modulates-beclin-1-lc3-and-p62-expression-to-2kqe49izpd.pdf

β‑asarone modulates Beclin‑1, LC3 and p62 expression to attenuate Aβ40 and Aβ42 levels in APP/PS1 transgenic mice with Alzheimer's disease.

Background
Autophagy has been reported to increase in cancer cells after radiation. However, it remains unknown whether increased autophagy as a result of radiation affects DNA damage repair and sensitizes cancer cells. In this study, the radiosensitization effect of rapamycin, a mammalian target of rapamycin inhibitor that induces autophagy, on human lung adenocarcinoma A549 cells was investigated.

https://onlinelibrary.wiley.com/doi/pdf/10.1111/1759-7714.12332

Rapamycin-induced autophagy sensitizes A549 cells to radiation associated with DNA damage repair inhibition.

The relationship between O-6-methylguanine-DNA methyltransferase (MGMT) promoter methylation and clinicopathological characteristics of non-small-cell lung carcinoma (NSCLC) has remained controversial and unclear. Therefore, in this study we have undertaken a systematic review and meta-analysis of relevant studies to quantitatively investigate this association. We identified 30 eligible studies investigating 2714 NSCLC patients. The relationship between MGMT hypermethylation and NSCLC was identified based on 20 studies, including 1539 NSCLC patient tissue and 1052 normal and adjacent tissue samples (OR = 4.60, 95% CI = 3.46~6.11, p < 0.00001). MGMT methylation varied with ethnicity (caucasian: OR = 4.56, 95% CI = 2.63~7.92, p < 0.00001; asian: OR = 5.18, 95% CI = 2.03~13.22, p = 0.0006) and control style (autologous: OR = 4.44, 95% CI = 3.32~5.92, p < 0.00001; heterogeneous: OR = 9.05, 95% CI = 1.79~45.71, p = 0.008). In addition, MGMT methylation was observed to be specifically associated with NSCLC clinical stage, and not with age, sex, smoking, pathological types, and differentiation status. Also MGMT methylation did not impact NSCLC patients survival (HR = 1.32, 95% CI = 0.77~2.28, p = 0.31). Our study provided clear evidence about the association of MGMT hypermethylation with increased risk of NSCLC.

/pdf/a-systematic-review-and-meta-analysis-association-between-3lzfpayouq.pdf

A systematic review and meta-analysis: Association between MGMT hypermethylation and the clinicopathological characteristics of non-small-cell lung carcinoma.

Background Radiotherapy is an important treatment for lung cancer. The poor prognosis of lung cancer is largely caused by the high recurrence rate and metastasis of the tumor. Autophagy, which can be induced by radiotherapy, might be associated with DNA repair. The aim of this study is to investigate whether activating autophagy using rapamycin can enhance the radiosensitivity of lung cancer cells and clarify the association of autophagy with DNA repair. Methods The human adenocarcinoma A549 cell line was selected as the experimental subject. The specimens were divided into three groups: control (N), radiation (R), and Rapamycin and radiation (R+RAPA). The protein levels of γ-H2AX, Rad51, Ku70/Ku80, p62, and LC3 were determined by Western blot. Autophagosome was observed under a transmission electron microscope, and SF was determined by colony formation assay. Results Compared with group R, the activity of autophagy and the protein expression levels of Rad51 and Ku70/80 were remarkably increased in group R+RAPA. Conclusions The radiosensitivity of lung cancer can be promoted by activating autophagy via treatment with Rapamycin, and the process may be associated with DNA repair. .

Role of Autophagy in the Radiosensitivity of Human Lung Adenocarcinoma A549 Cells

Background and objective It has been proven that cancer cell autophagy can be induced by hypoxia. In addition, autophagy was correlated with radiosensitivity. Thus, regulating the autophagy signaling pathway is a potential treatment strategy. The aim of this study is to investigate the effects of combined autophagy inhibitor 3-methyladenine (3-MA) on the radiosensitivity of human adenocarcinoma A549 cells in hypoxia condition. Methods A549 cells were cultured in hypoxia condition, and then divided into two groups: hypoxia group and 3-MA plus hypoxia group. Electronic microscopy was used to detect autophagosome levels at different time points. The expression of LC3 was examined by Western blot. The proliferation activity of A549 cells after radiotherapy (0 Gy, 2 Gy, 4 Gy, 6 Gy, 8 Gy, and 10 Gy) was determined with an MTT assay. Results Autophagosome formation and the LC3II/LC3I ratio increased under hypoxic conditions. After treatment with the autophagy inhibitor 3-MA, the quantity of autophagosomes and the LC3II/LC3I ratio decreased. The proliferative activity of the cells in the 3-MA plus hypoxia group was remarkably lower than that in the hypoxia group after treatment with radiotherapy. Conclusion The level of protective autophagy of A549 cells increased in hypoxia condition; thus, inhibiting autophagy improves the radiosensitivity of A549 cells.
	
	DOI: 10.3779/j.issn.1009-3419.2012.11.06

The effect of autophagy on the radioresistance of human adenocarcinoma A549 cell in hypoxia condition

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Rapamycin-induced autophagy sensitizes A549 cells to radiation associated with DNA damage repair inhibition.

A systematic review and meta-analysis: Association between MGMT hypermethylation and the clinicopathological characteristics of non-small-cell lung carcinoma.

Role of Autophagy in the Radiosensitivity of Human Lung Adenocarcinoma A549 Cells

The effect of autophagy on the radioresistance of human adenocarcinoma A549 cell in hypoxia condition