Wip1 is a nuclear protein and a member of serine/threonine specific protein phosphatase type 2C(PP2C)family.It was initially identified as a gene whose expression was induced in response to ? or UV radiation in a p53-dependent manner and a negative feedback regulation of p38MAPK-p53 signaling.Then,Wip1 gene was confirmed a proto-oncogene and amplified or overexpressed in several human tumor types.This review will introduce the structures and functions of Wip1 and details on the signaling process of cancer progression.

Objective To explore the relationship between lumbar disc degeneration (LDD) of lumbar spinal stenosis(LSS)and the dural sac cross-sectional area(DSCA)by MRI measurement. Methods 91 patients with central degenerative LSS were randomly selected and 91 age-and sex-matched people without LSS were select-ed as a control group. LDD was classified into five grades by MRI detection according to the method proposed by Pfirrmann and DSCA were measured. Results LDD was not associated with age in LSS. The proportion of severe degenerated disc in lower lumbar levels were higher than that of L2/3 in the two groups;DSCA in severe degenerat-ed disc group was significantly smaller than that in light degenerated group only in L2/3 and L3/4 in LSS. There were no statistical differences in every lumbar level in the control group. Conclusions LDD in L4/5 and L5/S1 of LSS is more severe than that of the normal people. DSCA and LDD are positively correlated in L2/3 and L3/4,but not in L4/5 and L5/S1 for LSS.

[Objective] The aim of this study was to establish a quantitative SYBR Green Ⅰ real-time PCR method for detection of wide-type p53-induced phosphatase 1 (Wip1 or PPM1D) gene expression level in non-small cell lung cancer (NSCLC),and to investigate the relationship between Wip1 mRNA expression level and the clinicopathological characters.[Method] Real-time PCR was employed to determine the expression level of Wip1 mRNA in 44 specimens of NSCLC tissues and their adjacent normal tissues.[Results] In the 44 specimens,the expression of Wip1 mRNA in both cancer tissues and adjacent normal lung tissues were positive.Wip1 gene was overexpressed in 17 specimens among 44 NSCLC specimens.The rate was 38.6%.The relative level of Wip1 mRNA in NSCLC tissues was significantly higher than the adjacent normal lung tissues (Ratio ＝ 2.1644 ± 1.394,P ＜ 0.01).The expression of Wip1 mRNA was also correlated with pathological staging (F ＝ 5.08,P ＝ 0.013).[Conclusion] The established SYBR Green Ⅰ quantitative real-time PCR method can successfully detect the expression level of Wip1 mRNA.The results suggested that Wip1 may be involved in the development of NSCLC.

Objective:To explore the effect of miRNA-511-3p (miR-511-3p) on the proliferation and apoptosis of lung cancer cells, and the possible role of ATP2A2 and endoplasmic reticulum stress therein.Methods:Lung cancer tissues and paracancerous normal tissues (>2 cm from the tumor) were retrospectively collected from 69 lung cancer patients who were admitted to Huizhou Central People's Hospital from January 2020 to March 2022. Real-time fluorescence quantitative polymerase chain reaction (qRT-PCR) was used to detect the transcript-level relative expression of miR-511-3p in cancer and paracancerous tissues, as well as immortalized lung epithelial cell line BEAS-2B, human lung cell line CCD-19Lu, and human lung carcinoma cell lines A549, H1975 and H1299. The lung cancer cell line A549 with the lowest relative expression level of miR-511-3p was selected for subsequent experiments. The cells were divided into miR control group (transfected with miR-511-3p irrelevant sequence), miR-511-3p overexpression group (transfected with miR-511-3p mimic), and miR-511-3p knockdown group (transfected with miR-511-3p repressor); and the additional A549 cells were taken and divided into ATP2A2 overexpression control group (transfected with its empty plasmid), ATP2A2 overexpression group (transfected with ATP2A2 overexpression plasmid), and ATP2A2 knockdown control group (transfected with irrelevant small interfering RNA plasmid) and ATP2A2 knockdown group (transfected with ATP2A2 small interfering RNA plasmid). The transcript-level relative expression of miR-511-3p and ATP2A2 in A549 cells in each group was detected by qRT-PCR; the relative expressions of ATP2A2 protein and endoplasmic reticulum stress marker proteins in each group were detected by Western blotting; the targeting relationship between miR-511-3p and ATP2A2 mRNA was verified by dual-luciferase reporter gene assay; CCK-8 assay was used to detect the proliferation ability of A549 cells in each group (expressed as absorbance value); flow cytometry was used to detect the percentage of apoptotic cells in A549 cells in each group; inorganic phosphorus colorimetry was used to detect the activity of Ca 2+-ATPase in A549 cells in each group; fluorescent probe assay was used to detect the Ca 2+ concentration in A549 cells in each group. Results:The transcript-level relative expression of miR-511-3p in lung cancer tissues and paracancerous tissues of 69 patients were 0.08±0.03 and 0.17±0.12, respectively, and the difference was statistically significant ( t= 6.04, P<0.05). The percentage of apoptotic cells in A549 cells in the miR-511-3p overexpression group, miR-511-3p knockdown group and miR control group was (58.1±6.1)%, (11.0±1.3)% and (22.0±2.1)%, respectively. The percentage of apoptotic cells in the miR-511-3p overexpression group was higher than that in the miR control group, and the percentage of apoptotic cells in the miR-511-3p knockdown group was lower than that in the control group, and the differences were statistically significant ( t values were 9.70 and 7.64, respectively, both P<0.05). After 24, 48 and 72 h of culture, the proliferation ability of A549 cells in the miR-511-3p overexpression group was lower than that in the miR control group, the proliferation ability of A549 cells in the miR-511-3p knockdown group was higher than that in the miR control group, and the differences were statistically significant (all P < 0.05). The percentage of apoptotic cells in A549 cells of ATP2A2 knockdown group and ATP2A2 knockdown control group were (58.2±1.5)% and (23.8±1.0)%, respectively, and the difference was statistically significant ( t= 33.94, P < 0.05); the percentage of apoptotic cells in A549 cells of ATP2A2 overexpression group and ATP2A2 overexpression control group were (13.8±2.0)% and (23.8±1.0)%, respectively, and the difference was statistically significant ( t= 7.96, P < 0.05). The transcript-level relative expression of ATP2A2 in A549 cells of miR-511-3p overexpression group was lower than that of miR control group, the transcript-level relative expression of ATP2A2 in A549 cells of miR-511-3p knockdown group was higher than that of control group, and the differences were statistically significant ( t values were 5.76 and 6.40, respectively, both P < 0.05); the relative expression of ATP2A2 protein in A549 cells of miR-511-3p overexpression group was lower than that of its control group, and the relative expression of ATP2A2 protein in A549 cells of miR-511-3p knockdown group was higher than that of its control group, and the differences were statistically significant (both P < 0.05). Dual-luciferase reporter gene assay verified the targeting relationship between miR-511-3p and ATP2A2 mRNA. The percentage of apoptotic cells in A549 cells in the control group, miR-511-3p overexpression group, ATP2A2 overexpression group, and miR - 511 - 3p overexpression+ ATP2A2 overexpression group were (21.5±3.0)%, (58.1±5.0)%, (13.3±1.2)%, and (20.5±4.0)%, respectively, and the difference was statistically significant (F= 73.28, P < 0.001); the percentage of apoptotic cells in A549 cells in the control group, miR-511-3p knockdown group, ATP2A2 knockdown group, and miR-511-3p knockdown+ ATP2A2 knockdown group were (23.5±3.0)%, (11.3±1.2)%, (60.1±7.0)%, and (25.6±5.0)%, respectively, and the difference was statistically significant ( F= 78.45, P < 0.001). The Ca 2+-ATPase activity in A549 cells of ATP2A2 overexpression group was higher than that of its control group, the Ca 2+-ATPase activity in A549 cells of ATP2A2 knockdown group was lower than that of its control group, and the differences were statistically significant ( t values were 4.61 and 6.07, respectively, both P < 0.05); the intracellular Ca 2+ concentration in A549 cells of ATP2A2 overexpression group was lower than that of its control group, the intracellular Ca 2+ concentration in A549 cells of ATP2A2 knockdown group was higher than that of its control group, and the differences were statistically significant ( t values were 3.30 and 3.95, respectively, both P < 0.05). The Ca 2+-ATPase activity in the miR-511-3p overexpression group was lower than that in the miR control group, the Ca 2+-ATPase activity in the miR- 511-3p knockdown group was higher than that in the miR control group, and the differences were statistically significant ( t values were 6.54 and 4.16, respectively, both P < 0.05); the intracellular Ca 2+ concentration in A549 cells of miR-511-3p overexpression group was higher than that of miR control group, the intracellular Ca 2+ concentration in A549 cells of miR - 511 - 3p knockdown group was lower than that of miR control group, and the differences were statistically significant ( t values were 3.60 and 6.23, respectively, both P < 0.05). The relative expressions of endoplasmic reticulum stress markers GRP78, PERK, p - eIF2a, ATF4, and CHOP proteins in A549 cells with knockdown of ATP2A2 or overexpression of miR-511-3p were higher than those in the corresponding control groups, and the differences were statistically significant (all P < 0.05); the relative expressions of all proteins in A549 cells with overexpression of ATP2A2 or knockdown of miR-511-3p were lower than those in the corresponding control groups (all P < 0.05). Conclusions:Changes in miR-511-3p level may affect the proliferation and apoptosis of lung cancer cells, and the mechanism may be that it affects the apoptosis of lung cancer cells by targeting ATP2A2 to regulate the endoplasmic reticulum stress.

OBJECTIVE: To investigate the computed tomography findings, clinicopathological features, genetic characteristics and prognosis of in situ adenocarcinoma (AIS) and minimally invasive adenocarcinoma (MIA) of the lung. METHODS: We retrospectively analyzed the data including computed tomography (CT) images, histopathological findings, Ki-67 immunostaining, and genetic mutations in patients with lung adenocarcinoma undergoing surgery at our hospital between 2014 and 2019. RESULTS: Of the total of 480 patients with lung adenocarcinoma we reviewed, 73 (15.2%) had AIS (=28) or MIA (=45) tumors. The age of the patients with MIA was significantly younger than that of patients with AIS ( < 0.02). CT scans identified pure ground-glass nodules in 46.4% of AIS cases and in 44.4% of MIA cases. Multiple GGOs were more common in MIA than in AIS cases ( < 0.05), and bluured tumor margins was less frequent in AIS cases ( < 0.05). No significant difference was found in EGFR mutations between MIA and AIS cases. A Ki-67 labeling index (LI) value ≥2.8% did not differentiate MIA from AIS. The follow-up time in MIA group was significantly shorter than that in AIS group, but no recurrence or death occurred. CONCLUSIONS Despite similar surgical outcomes and favorable survival outcomes, the patients with AIS and MIA show differences in terms of age, CT findings, EGFR mutations and Ki-67 LI.
Adenocarcinoma of Lung ; diagnostic imaging ; pathology ; ErbB Receptors ; genetics ; Humans ; Ki-67 Antigen ; genetics ; Lung Neoplasms ; diagnostic imaging ; pathology ; Mutation ; Prognosis ; Retrospective Studies ; Tomography, X-Ray Computed