Lung cancer: progression of heat shock protein 70 in association with flap endonuclease 1 protein.

Lung cancer is one of the leading causes of cancer deaths worldwide and existing approaches are not enough to manage, and hence, it is important to concentrate on new drug strategies. This study was aimed to identify the interacting partner of Flap endonuclease 1 (FEN1) and its role in cancer treatment. We identified a new FEN1 interacting partner confirmed it as Heat Shock Protein 70 (HSP 70), and its effect on FEN1 expression, in vitro. Additionally, we found that the 5-Fluorouracil's (5-FU) function was significantly improved when used in combination with HSP 70 inhibitor (KNK 437). The findings are interesting, elucidating the synergistic mechanism between two compounds which helps to develop a novel management strategy for over-expressed FEN1 in the lung. SUPPLEMENTARY INFORMATION: The online version contains supplementary material available at 10.1007/s13205-020-02598-3.

Construction and expression in vitro of a mifepristone inducible recombinant adenovirus carrying enhanced green fluorecence protein / 医学研究生学报

Objective To construct a mifepristone inducible recombinant adenovirus carrying enhanced green fluorecence protein for future gene therapy in vivo.Methods Full length red fluorescent gene and mifepristone regulator cassette was subcloned into PDC313 shuttle plasmid.The positive clone was identified by sequencing.Recombinant adenovirus were produced after cotransfection of the shutter vector PDC-EGFP and adenovirus DNA helper plasmid pBHGloxE1,3Cre into 293 cells.The recombined adenovirus was purified by CsCl density gradient centrifugation and its titer was determined by end point dilution assay.Fluorescence microscopy and FCM were confirmed by the activation of this regulatable recombinant adenovirus vector in infected cells.Results The adenovirus vector containing enhanced green fluorecence protein gene was identify by PCR.The virus titer of Ad-RUEGFP was 6.6?1010pfu/ml.Without the absence of mifepristone,no significant enhanced green fluorecence protein activation was observed,whereas in the presence of mifepristone activation of the enhanced green fluorecence protein was positive correlation with the inducer under definite range.Conclusion A replication-defective recombinant adenovirus vector containing enhanced green fluorecence protein was successfully constructed,which can be inducible by mifepristone.

Experimental study on arsenic trioxide-induced apoptosis of human pan creatic cancer cell line / 第二军医大学学报

Objective: To study the effect of arsenic trioxide (As2O3) on human pancreatic cancer cell proliferation and apoptosis (mainly early stage) in vitro. Methods: SW1990 cells line were trea ted with As2O3 at different concentration. Cell proliferation was evaluated by MTT and apoptosis by Annexin-Ⅴ-fluostaining, electron-microscopy, flow cytometry and immunocytochemical staining of Bcl-2 and Bax. Results: As2O3 and cisplatin had the same cytotoxity on SW1990. The cytotoxic effe ct on tumor cell was produced by induction of apoptosis. Twelve hours after cult ure with 10 μg/ml As2O3, much more SW1990 cells went into apoptosis than t he control. The apoptosis rate reached 24% after 48 h with the similar concentra tion of As2O3. Immunohistochemical study revealed that the expression of Bcl -2 was decreased after treated with As2O3. Conclusion: As 2O3 can depress the proliferation of SW1990 in vitro, mainly through the i nduction of apoptosis, and it is a potential agent for pancreatic cancer chemoth erapy.

Experimental study on arsenic trioxide induced apoptosis of human pancreatic cancer cell line / 第二军医大学学报

Objective: To study the effect of arsenic trioxide (As 2O 3) on human pancreatic cancer cell proliferation and apoptosis (mainly early stage) in vitro . Methods: SW1990 cells line were treated with As 2O 3 at different concentration. Cell proliferation was evaluated by MTT and apoptosis by Annexin Ⅴ fluostaining, electron microscopy, flow cytometry and immunocytochemical staining of Bcl 2 and Bax. Results: As 2O 3 and cisplatin had the same cytotoxity on SW1990. The cytotoxic effect on tumor cell was produced by induction of apoptosis. Twelve hours after culture with 10 ?g/ml As 2O 3, much more SW1990 cells went into apoptosis than the control. The apoptosis rate reached 24% after 48 h with the similar concentration of As 2O 3. Immunohistochemical study revealed that the expression of Bcl 2 was decreased after treated with As 2O 3. Conclusion: As 2O 3 can depress the proliferation of SW1990 in vitro , mainly through the induction of apoptosis, and it is a potential agent for pancreatic cancer chemotherapy.