Abstract
In cancer research, autophagy has been revealed as one of the major ways to maintain the metabolism of cancer cells, including glioma cells, through protein degradation. Meanwhile, autophagy is also regarded as a kind of mechanism to protect glioma cells from a harmful stimulus, such as chemical and radiation treatment. So, the inhibition of autophagy may be very helpful in curing glioma. This study aimed to determine the effect of autophagic inhibition on glioma cells using tubacin, a specific inhibitor of histone deacetylase 6(HDAC6). According to the results, tubacin inhibited the growth of both U251 and LN229 cells, which was accompanied by lower HDAC6 activity and accumulated autophagosome. The inhibition of HDCA6 also led to accumulation of autophagosome and death of glioma cells. Moreover, the combined treatment of tubacin and temozolomide, an alkylating agent used to treat glioblastoma, induced more severe glioma cell death. Thus, it can be concluded that inhibition of HDAC6 suppressed growth and drug resistance of glioma cells in-vitro through autophagic suppression and blocking of fusion of autophagosome and lysosome.
Highlights
Among the primary central nervous system (CNS) tumors, 40% are glial neoplasms
The results showed that HDAC6 expression in tumor tissue from these patients was higher than in the control,whereas the average level of HDAC6 mRNA in tumor tissues was high compared with adjacent tissue of tumor from single patients as shown in Fig. 1A and B
We found that tubacin could inhibit the activity of HDAC6 and suppress autophagy
Summary
Among the primary central nervous system (CNS) tumors, 40% are glial neoplasms. According to the histopathological and clinical features identified by the World HealthOrganization (WHO), these neoplasms are classified into four grades [1]. Among the primary central nervous system (CNS) tumors, 40% are glial neoplasms. According to the histopathological and clinical features identified by the World Health. Organization (WHO), these neoplasms are classified into four grades [1]. High-grade gliomas, including glioblastoma multiforme (GBM) and anaplastic astrocytoma, threaten health most. Histological features of glioblastoma are marked by vascular proliferation, high cell density with mitotic activity and aggressive invasion into normal brain tissue [2]. Surgical resection followed by radiation and temozolomide treatment is the most frequent strategy used clinically to cure patients with glioma. Radiation and temozolomide treatment can induce protective autophagy to prevent excessive death of glioma cells [3]
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