Astragaloside IV sensitizes non-small cell lung cancer cells to gefitinib potentially via regulation of SIRT6.

Astragaloside IV, the active component of Astragalus membranaceus, exhibits diverse biological roles including the anti-tumor activity. In this study, we evaluated the chemosensitive role of astragaloside IV in non-small cell lung cancer cells. Cell Counting Kit-8 analysis was performed to determine cell viability. Real-time polymerase chain reaction and western blot were used to measure the messenger RNA and protein expression. Results showed that astragaloside IV treatment could suppress the proliferation of non-small cell lung cancer cells. In addition, combined treatment with astragaloside IV remarkably enhanced the chemosensitivity to gefitinib in three non-small cell lung cancer cell lines including NCI-H1299, HCC827, and A549. Furthermore, compared with gefitinib-treated cells, the messenger RNA expression of SIRT6 was obviously increased in non-small cell lung cancer cells treated with gefitinib combined with astragaloside IV. In addition, downregulation of SIRT6 was accomplished using small interference RNA technology. As a result, SIRT6 inhibition abolished the sensitization role of astragaloside IV in non-small cell lung cancer cells. Taken together, these data demonstrated that astragaloside IV sensitized tumor cells to gefitinib via regulation of SIRT6, suggesting that astragaloside IV may serve as potential therapeutic approach for lung cancer.

[Influencing Mechanism of Eh, pH and Iron on the Release of Arsenic in Paddy Soil].

The massive release of soil arsenic and its enrichment in rice are significantly associated with the flooded and anaerobic management in paddy soil. Soil redox potential (Eh), pH and iron oxides exert remarkable impacts on arsenic release, which remain to be explored. In this study, long-term aerobic and anaerobic as well as intermittent aerobic incubation treatments were applied to investigate the influences of Eh, pH and iron content on arsenic release. It was found that anaerobic and flooded treatment contributed to the highest arsenic release. With decreasing Eh, significant enhancement in As(Ⅲ) and As(Ⅴ) contents in soil solution was observed. Particularly, As(Ⅲ) and As(Ⅴ) contents during the second phase increased by 1.37 and 0.99 µg·L-1compared with those in the first phase. Conversely, significant reduction in soil arsenic release (P<0.05) occurred when intermittent aerobic treatment was adopted, and the lowest level of arsenic release was observed along with the longest treatment time (6 d). The exponent relationships between arsenic and soil Eh, pH and Fe2+ content were also established, which indicated that arsenic release could be accelerated by lower pH and elevated Eh. In addition, a significant positive correlation was also found between iron(Ⅱ) content and arsenic content in soil solution. Since low Eh and elevated pH served as critical factors driving arsenic release, intermittent and aerobic water management was proved to be an effective method for the inhibition of arsenic release and uptake and accumulation of arsenic by rice.

miR-630 targets LMO3 to regulate cell growth and metastasis in lung cancer.

MicroRNAs (miRNAs) are a class of small non-coding RNAs that play key roles in cancer development and progression. Therefore, the discovery of miRNAs may provide a new and powerful tool for understanding the mechanism of carcinogenesis. In the present study, we aimed to investigate the functional significance of miR-630 and to identify its possible target genes in human non-small cell lung cancer (NSCLC). Our results showed that miR-630 was significantly down-regulated in NSCLC tissues and cell lines. The enforced expression of miR-630 was able to inhibit cell proliferation, migration, and invasion of NSCLC cells. Moreover, our results further revealed that LMO3, a nuclear LIM-only proteins, was identified as a target of miR-630. Restoration of LMO3 remarkably reversed the tumor-suppressive effects of miR-630 on cell proliferation, migration, and invasion in NSCLC cells. Therefore, we demonstrated that miR-630 suppressed the proliferation, migration, and invasion of NSCLC cells by down-regulating LMO3 expression, suggesting miR-630 as a potential therapeutic target for the treatment of human NSCLC in the future.

[Pulmonary cryptococcosis: analysis of 38 cases].

OBJECTIVE: To investigate the clinical features, radiology, diagnosis and treatment of pulmonary cryptococcosis. METHODS: A total of 38 cases of pulmonary cryptococcosis, confirmed by pathological examinations at Fuzhou General Clinical Medical College, Fujian Medical University from March 2003 to February 2010, were retrospectively studied. RESULTS: All of the cases were community-acquired. The patients consisted of 29 males and 9 females, aged from 21 to 70 years. There were no underlying diseases in 29 cases. The CD(4) cell numbers were normal in 20 patients. Radiological study showed that the majority of the lesions (35 cases) were close to the pleura. Lower lungs were often involved (left 21 and right 23). Pulmonary nodules, either solitary nodules (11 cases) or multiple nodules (16 cases), were the most common CT finding. The lesions had a higher standardized uptake value (SUV) in 4 patients with a PET-CT scan. The lung specimens of 33 cases were obtained by CT guided transthoracic needle aspiration biopsy. The disease was cured in 34 cases, and improved in 3 cases, but 1 died. CONCLUSIONS: Pulmonary cryptococcosis must be considered in the differential diagnosis of lesions of the lungs. The disease has some characteristics on radiology, such as multiple lesions, always close to the pleura and occurs frequently in the lower lungs. CT guided percutaneous biopsy is a safe and effective method for diagnosis.

[An experimental study on the safety of intratracheal drug administration].

OBJECTIVE: To explore whether injury and repair occur in the trachea and the lung after intra-tracheal administration of different drugs. METHODS: Wistar rats were randomly divided into 5 groups, a normal group, a blank control (BC) group, a normal saline (NS) group, a lidocaine (LD) group and an amikacin (AK) group. For the latter 3 groups, normal saline, lidocaine and amikacin were injected into trachea by needle puncture. Scanning electron microscope was used to observe the ultra-structural changes of the epithelium, and the percentage of the area of damage (PAD) in tracheal mucosa was calculated. Moreover, pathological changes of the mucous membrane of bronchioles and alveolar epithelial cells were also examined, and the degree of lung pathology was semi-quantified. RESULTS: Two hours after the injection of the 3 drugs, derangement and edema of the cilia were evident by scanning electron microscopy. The PAD of the NS group, the LD group and the AK group were (94.2 ± 3.2)%, (93.1 ± 3.0)% and (95.5 ± 1.8)%, respectively; all being significantly higher than that of the BC group (1.3 ± 0.3)%. For the NS group and the LD group, the PAD decreased significantly after 24 h, which were (73.7 ± 7.8)% and (81.0 ± 4.6)% respectively, and returned to normal at 48 h and 96 h. While for the AK group, the damage began to improve at 72 h [PAD (62.1 ± 5.2)%], and recovered at 96 h. Airway epithelial derangement and cell edema in the alveoli and the bronchioles also occurred 2 h after drug injection, and inflammatory cell infiltration became evident at 24 h. At this time, the score of pathology was 1.80 ± 0.84, 2.60 ± 0.55 and 2.80 ± 0.45 for the NS group, the LD group and the AK group, respectively; all being higher than that of the BC group (0). These pathological changes recovered totally after 72 h for the NS and the LD groups, and 96 h for the AK group. CONCLUSIONS: Intra-tracheal administration of normal saline, lidocaine and amikacin in rats led to reversible airway mucosal and lung tissue damages.

Inhibition of lung adenocarcinoma LA795 in mice by recombinant human endostatin.

OBJECTIVE: To evaluate the inhibitory effect of recombinant human endostatin on tumor growth and metastasis of adenocarcinoma LA795 in mice. METHODS: Recombinant human endostatin was purified rom endostadin-expressing pCX clones. LA795 cells were inoculated subcutaneously on the back of T739 mice, which were randomized into 2 groups. From the tenth day on, treatment group was given 20 mg/kg recombinant human endostatin subcutaneously daily for 14 consecutive days, and the control group received PBS in the same manner. The sizes of the subcutaneous tumors, lung weights, the number of metastases over the lung surface and the survival time of the mice were observed. RESULTS: The tumor sizes of the treatment group in creased slowly from (650+/-201) mm3 to (1 642+/-21) mm3 when compared with those of the control group which showed and increase from (623+/-248) mm3 to (9 194+/-952) mm3. The lung weight of the 2 groups was (190+/-25) mg and (324+/-43) mg respectively, and the number of lung sung surface metastases was 8+/-2 and 22+/-8 for each. The average survival time of the rats in the 2 groups was 48 d and 27 d, respectively. All parameters measured between the 2 groups showed significant differences (P<0.01). CONCLUSION: Recom binent human endostatin has strong inhibitory effect on both the growth of primary tumor and metastasis of lung adenocarcinoma LA795 cells, and prolongs the survival time of the tumor-bearing mice.