Effectiveness of sarcopenia screening markers in predicting out-of-hospital death in the oldest (≥80 years) older.

OBJECTIVE: The goal of this investigation was to elucidate the correlation between sarcopenia screening indicators (aspartate transaminase/alanine transaminase (AST/ALT) and creatinine/cystatin C*100 (Cr/CysC*100)) and the risk of out-of-hospital (OFH) death among the very advanced age (≥80 years) population. METHODS: We conducted a retrospective cohort investigation, involving internal medicine inpatients aged ≥80 years of age, who sought treatment at a teaching hospital in western China. We obtained OFH mortality information from telephonic interviews. Subsequently, we employed Cox proportional hazards models to analyze the links between AST/ALT and Cr/CysC*100 and OFH all-cause mortality among the very advanced age (≥80 years old) population. RESULTS: In all, we recruited 398 subjects, among which 51.51% were male. The median age of OFH deceased male patients was 85 years, and the same for female patients was 87 years. The total quantity of OFH deaths was 164 (41.21%). Among the oldest male population, those who died OFH exhibited enhanced AST/ALT, relative to those who survived (death vs. survival: 1.5 vs 1.3, P=0.008). However, among the oldest female, there was no difference in AST/ALT between patients who expired OFH, and those who survived. Among the oldest elders (male and female), Cr/CysC*100 did not significantly differ between surviving and OFH deceased patients. Additional analysis involving the Cox proportional hazards model revealed that among the oldest male population, an enhanced AST/ALT denoted an augmented risk of OFH death (hazard ratios (HRs) =1.797, 95%CI: 1.2-2.691). However, Cr/CysC*100 was not correlated with OFH mortality risk. Among the oldest female population, neither AST/ALT nor Cr/CysC*100 was correlated with OFH mortality risk. CONCLUSIONS: Enhanced AST/ALT was correlated with an augmented OFH mortality risk among the oldest male, but not female population. Alternately, Cr/CysC*100 was not linked to OFH mortality risk among any population.

The Effectiveness and Rotational Stability of Vertical Implantation of the Implantable Collamer Lens for the Treatment of Myopia.

PURPOSE: To explore the effectiveness and rotational stability of vertical implantation of the Implantable Collamer Lens (ICL) (STAAR Surgical) to treat myopia. METHODS: This was a prospective, randomized, controlled study, including 78 eyes from 46 patients with myopia who underwent ICL implantation. The patients were randomly divided into vertical and horizontal implantation groups. At 1 day, 1 week, 1 month, and 3 months after surgery, rotational stability was evaluated using the postoperative axis deviation from the intended axis by the digital anterior segment photograph. The vault, crystalline lens rise, anterior chamber depth, manifest refraction spherical equivalent, intraocular pressure, and visual acuity values were obtained before and after surgery. RESULTS: A 3-month follow-up period showed significant differences between the efficacy indexes in the horizontal (1.11 ± 0.02) and vertical (1.13 ± 0.02) groups (P = .455). No significant difference was observed in the postoperative manifest refraction spherical equivalent between the horizontal (-0.27 ± 0.18 diopters) and vertical (0.01 ± 0.08 diopters) groups (P = .151). Also, no statistically significant difference was observed in the corneal endothelial cells and intraocular pressure between groups (P = .555, P = .464). The rotation angle of the horizontal group was greater at 1 week, 1 month, and 3 months (3.14° ± 2.13°, 2.97° ± 2.01°, 3.27° ± 2.12°, respectively) compared to that of the vertical group (1.30° ± 1.29°, 1.85° ± 1.60°, 1.74° ± 1.33°, respectively) (P < .001 for all). From 1 week to 3 months, the changing angle of horizontal (0.31° ± 1.86°) and vertical (0.49° ± 1.33°) ICL rotation displayed a positive correlation with the changing vault of horizontal (48.41 ± 86.02 mm) and vertical (39.64 ± 78.43 mm) ICL rotation (r = 0.242, 0.335, P = .033, .037). CONCLUSIONS: The study supports great efficacy and safety in both vertical and horizontal implantation, with the vertical implantation group displaying better stability. [J Refract Surg. 2022;38(10):641-647.].

Optimizing the IPSA Conditions to Improve the Treatment Plan Quality in Brachytherapy for Cervical Cancer.

Recent prevalent use of three-dimensional image-guided brachytherapy (3D brachytherapy) has dramatically improved the treatment outcomes of cervical cancer. Inverse planning simulated annealing (IPSA) is one of the commonly used algorithms in 3D brachytherapy, but different conditions may affect the treatment plan quality. In this study, we compared HRCTV (high-risk clinical target volume) D90 (dose prescription) and HRCTV D95 D2cc (dose received by 2.0cc) of the rectum, bladder, and sigmoid in 30 patients with cervical cancer under four IPSA conditions. The HRCTV D90 (mean ± SD cGy) was 607.32 ± 37.86, 599.01 ± 23.62, 598.67 ± 13.07, and 596.45 ± 10.94 in four groups, respectively. The HRCTV D95 was 558.19 ± 38.51, 558.17 ± 25.72, 557.03 ± 16.12, and 555.26 ± 12.78, respectively. The sigmoid D2cc was 282.96 ± 44.84, 273.14 ± 60.69, 268.94 ± 62.32, and 292.69 ± 52.44. HRCTV D90, HRCTV D95, and sigmoid D2cc were not statistically different among the four groups (p > 0.05). However, the target fitness in group one, especially at the cervix, was poor. The rectum D2cc was 351.49 ± 32.90, 361.49 ± 28.09, 370.82 ± 24.44, and 375.33 ± 30.90. The rectum D2cc in group one was the lower than that in group three and group four (p < 0.05). The bladder D2cc was 423.59 ± 31.39, 380.75 ± 37.25, 383.27 ± 32.55, and 385.22 ± 25.79. The bladder D2cc in group one was higher than the other groups (p < 0.05). The maximum rectum limit dose (400cGy) is lower than the bladder (500cGy), and HRCTV is a whole in the IPSA algorithm; these result in the insufficiency or even absence of cervix dose that first need to meet in clinics. In conclusion, IPSA condition optimization can improve the quality of treatment plan in 3D brachytherapy and make it closer to clinical practice.

An Adversarial Deep-Learning-Based Model for Cervical Cancer CTV Segmentation With Multicenter Blinded Randomized Controlled Validation.

PURPOSE: To propose a novel deep-learning-based auto-segmentation model for CTV delineation in cervical cancer and to evaluate whether it can perform comparably well to manual delineation by a three-stage multicenter evaluation framework. METHODS: An adversarial deep-learning-based auto-segmentation model was trained and configured for cervical cancer CTV contouring using CT data from 237 patients. Then CT scans of additional 20 consecutive patients with locally advanced cervical cancer were collected to perform a three-stage multicenter randomized controlled evaluation involving nine oncologists from six medical centers. This evaluation system is a combination of objective performance metrics, radiation oncologist assessment, and finally the head-to-head Turing imitation test. Accuracy and effectiveness were evaluated step by step. The intra-observer consistency of each oncologist was also tested. RESULTS: In stage-1 evaluation, the mean DSC and the 95HD value of the proposed model were 0.88 and 3.46 mm, respectively. In stage-2, the oncologist grading evaluation showed the majority of AI contours were comparable to the GT contours. The average CTV scores for AI and GT were 2.68 vs. 2.71 in week 0 (P = .206), and 2.62 vs. 2.63 in week 2 (P = .552), with no significant statistical differences. In stage-3, the Turing imitation test showed that the percentage of AI contours, which were judged to be better than GT contours by ≥5 oncologists, was 60.0% in week 0 and 42.5% in week 2. Most oncologists demonstrated good consistency between the 2 weeks (P > 0.05). CONCLUSIONS: The tested AI model was demonstrated to be accurate and comparable to the manual CTV segmentation in cervical cancer patients when assessed by our three-stage evaluation framework.

Hsa_circ_0102171 aggravates the progression of cervical cancer through targeting miR-4465/CREBRF axis.

Cervical cancer (CC) has caused numerous cancer-related deaths in women. Recent years, circular RNAs have been reported as vital factors in CC tumorigenesis. Our current study focused on the role of hsa_circ_0102171 (called circ_0102171 subsequently) in CC. At first, we applied reverse transcription polymerase chain reaction to detect the expression of circ_0102171 in CC tissues and cells. Subsequently, we silenced circ_0102171 to conduct loss-of-function assays, including cell counting kit-8 assay, 5-ethynyl-2'-deoxyuridine staining, Transwell assay, and flow cytometry analysis. Interestingly, we discovered that circ_0102171 expressed at a high level in CC tissues and cells. Functionally, silencing circ_0102171 prohibited cell proliferation, migration and invasion, and strengthened cell apoptosis in CC in vitro. Mechanistic investigations revealed that circ_0102171 could act as a sponge for miR-4465. Gain-of-function assays demonstrated that miR-4465 hindered the growth and migration of CC cells. Moreover, circ_0102171 enhanced the level of CREB3 regulatory factor (CREBRF) which was the downstream target of miR-4465. Rescue assays suggested that CREBRF and miR-4465 could involve in circ_0102171-mediated CC progression. Finally, in vivo data supported that silencing circ_0102171 hindered CC cell growth. In conclusion, circ_0102171 aggravates CC progression via targeting miR-4465/CREBRF axis.

Dose fusion and efficacy evaluation of different radical radiotherapy doses for cervical cancer.

BACKGROUND: The recommended external beam radiotherapy (EBRT) dose for cervical cancer is 40-50 Gy, but there is no consensus. In this study, 45-Gy and 50.4-Gy treatment groups were compared for fused doses to target tumor areas and organs at risk (OARs), clinical efficacy, and quality of life. METHODS: Seventy-nine cases receiving radical radiotherapy within the past 3 years were retrospectively analyzed. EBRT and three-dimensional brachytherapy dose fusion values were calculated for target areas and OARs using Elastix V5.0. Clinical efficacy was assessed using Response Evaluation Criteria in Solid Tumors (RECIST), adverse events using Common Terminology Criteria for Adverse Events v4.03 (CTCAE4.03), and quality of life using the European Organization for Research and Treatment of Cancer Quality of Life Questionnaire-Core 30 (EORTC QLQ-C30). RESULTS: Minimum fused dose delivered to 90% of the high-risk clinical target volume (HRCTV D90) did not differ significantly between 45-Gy and 50.4-Gy groups, whereas D2cc values of rectum and bladder (OARs) were significantly lower in the 45-Gy group (both p < 0.05). Further analysis showed that these D2cc differences resulted primarily from EBRT. No grade III-IV adverse events were observed in either group during follow up. Short-term clinical efficacy, adverse events, and EORTC QLQ-C30 functional and symptom scales also did not differ significantly between groups (all p > 0.05). However, quality of life was markedly higher in the 45-Gy group (p < 0.05). CONCLUSION: Appropriate EBRT dose reduction can reduce OAR irradiation without compromising total target area dose or clinical efficacy. Dose fusion can facilitate the judicious choice of EBRT to limit OAR exposure, reduce adverse events, and enhance the quality of life.

LINC02535 co-functions with PCBP2 to regulate DNA damage repair in cervical cancer by stabilizing RRM1 mRNA.

Cervical cancer (CC) is one of the commonest malignant cancers among women with high morbidity and mortality. Despite encouraging advances had been found in diagnostic and therapeutic strategies, effective therapeutic strategy and further exploration of the mechanism underlying in CC is still needed. We searched The Cancer Genome Atlas database and found that long noncoding RNA LINC02535 was highly expressed in CC. LINC02535 has not been studied in CC, and its molecular regulation mechanism remains unknown. Based on starBase database, LINC02535 could potentially bind poly (rC) binding protein 2 (PCBP2). In the present study, we discovered a significant increase of the LINC02535 and PCBP2 expression in CC tissues and cells as compared with the adjacent normal tissues and normal cervical epithelial cells. LINC02535 and PCBP2 can bind with each other and were colocated in cytoplasm. LINC02535 and PCBP2 promoted cell proliferation, migration, invasion, and suppressed apoptosis in CC. LINC02535 and PCBP2 facilitated the repair of DNA damage to promote CC progression. LINC02535 cooperated with PCBP2 to enhance the stability of RRM1 messenger RNA (mRNA). RRM1 promoted the repair of DNA damage and epithelial-to-mesenchymal transition (EMT) process in CC cells. LINC02535 regulated tumorigenesis in vivo. In conclusion, LINC02535 cooperated with PCBP2, regulated stability of RRM1 mRNA to promote cell proliferation and EMT process in CC cells by facilitating the repair of DNA damage, providing a potential biomarker for CC.

Effect of hypothermic perfusion on phacoemulsification in eyes with hard nuclear cataract: randomized trial.

PURPOSE: To evaluate the effectiveness and safety of hypothermic perfusion in the phacoemulsification of hard nuclear cataract. SETTING: Tertiary opthalmology center, China. DESIGN: Laboratory study and prospective randomized clinical trial. METHODS: Rabbits and patients with hard nuclear cataract underwent phacoemulsification with perfusion temperatures at 4°C or 24°C. Anterior segment optical coherence tomography (AS-OCT), corneal endothelial cell count (ECC), and cornea sections were observed before the rabbits' operation and 1 day and 7 days postoperatively. AS-OCT, corneal ECC, and anterior chamber (AC) inflammation were observed before the patients' operation and 1 day, 7 days, and 30 days postoperatively. RESULTS: The study comprised 40 rabbits and 80 patients. In the animal models, the mean central corneal thickness (CCT) in the 4°C group (370.4 µm ± 45.5 [SD]) was thinner than in the 24°C group (496.7 ± 121.5 µm) 1 day postoperatively (P < .001). The mean AC inflammation reaction grade in the 4°C group (1.1 ± 0.9) was lower than in the 24°C group (2.2 ± 0.8) (P = .0333). In clinical trials, the mean CCT and incisional corneal thicknesses in the 4°C group (600.7 ± 51.8 µm and 859.2 ± 177.8 µm, respectively) were thinner than in the 24°C group (655.3 ± 85.0 µm and 955.9 ± 196.7 µm, respectively) (P < .001). The endothelial cell density (P = .036) and hexagonality (P = .001) were higher in the 4°C group. The mean AC inflammation reaction grade in the 4°C group (0.6 ± 0.6) was lower than in the 24°C group (1.3 ± 1.0) 1 day postoperatively (P = .004). CONCLUSIONS: Hypothermic perfusion in phacoemulsification of hard nuclear cataract is safe and it can effectively protect corneal endothelium, decrease corneal edema, and reduce AC inflammation in the early postoperative stage.

Pseudogene RACGAP1P activates RACGAP1/Rho/ERK signalling axis as a competing endogenous RNA to promote hepatocellular carcinoma early recurrence.

Accumulating evidence has indicated crucial roles for pseudogenes in human cancers. However, the roles played by pseudogenes in the pathogenesis of HCC, particularly HCC early recurrence, still incompletely elucidated. Herein, we identify a novel early recurrence related pseudogene RACGAP1P which was significantly upregulated in HCC and was associated with larger tumour size, advanced clinical stage, abnormal AFP level and shorter survival time. In vitro and in vivo experiments have shown that RACGAP1P is a prerequisite for the development of malignant characteristics of HCC cells, including cell growth and migration. Mechanistic investigations indicated that RACGAP1P elicits its oncogenic activity as a ceRNA to sequestrate miR-15-5p from its endogenous target RACGAP1, thereby leading to the upregulation of RACGAP1 and the activation of RhoA/ERK signalling. These results may provide new insights into the functional crosstalk of the pseudogene/miRNA/parent-gene genetic network during HCC early relapse and may contribute to improving the clinical intervention for this subset of HCC patients.

p68 prompts the epithelial-mesenchymal transition in cervical cancer cells by transcriptionally activating the TGF-ß1 signaling pathway.

Overexpression of p68 has been reported in various types of cancer. However, little study has been conducted on the expression and role of p68 in cervical cancer. Therefore, the present study focuses on the role of p68 in cervical cancer cells, which may elucidate its potential mechanism of cervical cancer progression and shed light on the precision medical treatment of cervical cancer. Firstly, the expression of p68 was analyzed using reverse transcription-quantitative polymerase chain reaction and western blot analysis. The changes to cell morphology were observed using an inverted microscope (XDS-500D; Shanghai Caikon Optical Instrument Co., Ltd., Shanghai, China). Cell migration was determined using an in vitro scratch assay. The present study demonstrated that the mRNA and protein levels of p68 were significantly enhanced in cervical cancer CaSki, HeLa [human papillomavirus (HPV)-18-positive], SiHa (HPV-16-positive) and C-33A (HPV-negative) cell lines compared with the human keratinocyte HaCaT cell line. Overexpression of p68 induced an elongated and spindle-shaped morphology in CaSki cells. Upregulation of p68 increased the expression of α-smooth muscle actin, vimentin and fibronectin however, epithelial marker E-cadherin was significantly decreased. Furthermore, the in vitro scratch assay demonstrated that overexpression of p68 markedly enhanced CaSki cell migration capacity at 24 and 48 h. Knockdown of p68 partially reversed transforming growth factor-ß1 (TGF-ß1)-induced changes in epithelial-mesenchymal transition (EMT) markers and cell morphological changes. In summary, the present study demonstrated that p68 transcriptionally activated the expression of TGF-ß1, thereby prompting EMT in cervical cancer cells.

Radiotherapy induces cell cycle arrest and cell apoptosis in nasopharyngeal carcinoma via the ATM and Smad pathways.

Nasopharyngeal carcinoma (NPC) is a common malignant neoplasm of the head and neck which is harmful to human's health. Radiotherapy is commonly used in the treatment of NPC and it induces immediate cell cycle arrest and cell apoptosis. However, the mechanism remains unknown. Evidences suggested the activation of Ataxia telangiectasia mutated (ATM) pathway and Smad pathway are 2 of the important crucial mediators in the function of radiotherapy. In this study, we performed in vitro assays with human nasopharyngeal carcinoma CNE-2 cells and in vivo assays with nude mice to investigate the role of the ATM and Smad pathways in the treatment of nasopharyngeal carcinoma with radiotherapy. The results suggested that radiation induced activation of ATM pathway by inducing expression of p-ATM, p-CHK1, p-CHK2, p15 and inhibiting expression of p-Smad3. In addition, Caspase3 expression was increased while CDC25A was decreased, leading to cell cycle arrest and cell apoptosis. On the other hand, activation of Smad3 can inhibited the ATM pathway and attenuated the efficacy of radiation. In summary, we suggest that both ATM and Smad pathways contribute to the cell cycle arrest and cell apoptosis during nasopharyngeal carcinoma cells treated with radiation.

Laparoscopic resection of primary adrenal ganglioneuroma: A case report and review of the literature.

Adrenal ganglioneuroma (AGN) is an extremely rare, benign tumor that originates from the neural crest tissue of the sympathetic nervous system. The majority of cases are detected incidentally, since the disease often lacks clear clinical manifestations or is asymptomatic. In addition, AGN is often misdiagnosed as being an adrenal adenoma or adrenal pheochromocytoma. The present study describes a 58-year-old female who visited the outpatient clinic of the Affiliated Hospital of Guangdong Medical College (Zhanjiang, Guangdong, China) with symptoms of face and lower extremity dropsy. Color Doppler ultrasonography revealed a solid tumor in the right kidney, and abdominal computed tomography identified an irregular, solid tumor measuring ~6×4.5×7 cm3 and arising from the right adrenal gland, with a clear boundary. Magnetic resonance imaging was not performed. An initial diagnosis of adrenal adenoma was established. The patient was treated by laparoscopy in order to remove the tumor. However, following surgery, a pathological examination suggested that the tumor was a GN originating from the adrenal medulla. The formation of a correct diagnosis can be extremely challenging, as AGNs do not exhibit any specific clinical manifestations. Therefore, detection often depends entirely upon imaging studies, and the final diagnosis can be only by confirmed following a histopathological evaluation.

Surgical resection and post-operative radiotherapy in an adult renal neuroblastoma patient with multiple bone and joint metastases: A case report.

Renal neuroblastoma is uncommon, particularly in adults, with only a few cases having been reported in studies published in the English language. The incidence is only 0.12 cases/1 million individuals in those aged >20 years. Studies of the pathogenesis, biological characteristics, treatment and prognosis of renal neuroblastoma are limited due to this low incidence. The present study reports the case of a 22-year-old adult female who was diagnosed with a left renal neuroblastoma by computed tomography (CT), bone scan and pathological examination. The patient underwent a left nephroureterectomy, ipsilateral lymph node dissection and post-operative radiotherapy, prior to discharge 60 days after admittance. At the nine-month follow-up examination, the patient showed no evidence of recurrence, progression or metastatic disease on the CT scans of the chest, abdomen and pelvis. Renal neuroblastoma is extremely uncommon in adults. The diagnosis and treatment of renal neuroblastoma is complicated by the overall low incidence, lack of specific treatment guidelines, advanced disease state due to late presentation, and its associated co-morbidities. Further study of the pathogenesis, biological and clinical characteristics, and treatment of renal neuroblastoma is required to provide an optimal treatment for patients and to improve the patient's quality of life.

Overexpressed GRP78 affects EMT and cell-matrix adhesion via autocrine TGF-ß/Smad2/3 signaling.

Glucose-regulated protein of 78kD (GRP78) is a multifunctional protein belonging to the heat shock protein 70 family. Overexpression of GRP78 triggered by environmental and physiological stresses is positively correlated with the occurrence and progression of various tumors, but the molecular mechanisms have not been well established. The present study indicated that overexpression of GRP78 in colon cancer cells could promote cell-matrix adhesion through the upregulation of fibronectin, integrin-ß1 and phosphorylated FAK. Meanwhile, it resulted in a visible epithelial-mesenchymal transition in DLD1 cells, and the Snail-2 played the key role during the process. More importantly, the data indicated that GRP78 overexpression facilitated the expression and secretion of TGF-ß1, which further activated the downstream Smad2/3 signaling module to effectuate the cell-matrix adhesion and epithelial-mesenchymal transition. Taken together, this study provides a novel molecular mechanism involving in the effects of GRP78 on colon cancer metastasis.

Small cell carcinoma of the urinary bladder: A case report and review of the literature.

Small cell carcinoma of the urinary bladder (SCBC) is a type of rare malignant tumor of the urinary tract. As it does not have specific symptoms and its epidemiological features are similar to transitional cell carcinoma of the bladder, it is often misdiagnosed. SCBC is highly aggressive, metastasizes very early and has a poor prognosis, and consequently, it has become a focus for urological surgeons and oncologists. An 82-year-old male visited the Department of Urinary Surgery, in the Affiliated Hospital of Guangdong Medical College (Zhanjiang, China), due to gross hematuria that had persisted for one week. Abdominal computed tomography showed a neoplasm of ~6×6×7 cm on the anterior wall of the bladder. The initial diagnosis was of uroepithelial cell carcinoma of the bladder and surgery was performed to remove the tumor. However, the subsequent pathological examination suggested that the tumor was an SCBC. Small cell carcinoma is a highly malignant disease, with a high mortality rate, and it rarely occurs in the bladder. Upon review of a large number of studies, SCBC was not found to present with specific symptoms, making the early diagnosis of the disease difficult, however, commonly occurring symptoms included dysuria, painless gross hematuria and urinary tract obstruction.

Effect of stable transfection with PHD3 on growth and proliferation of HepG2 cells in vitro and in vivo.

OBJECTIVE: To establish a human hepatoma HepG2 cell line with stable expression of Prolyl hydroxylase domain 3 (PHD3) gene and study its effect of growth and proliferation in nude mice xenograft tumor. METHODS: Eukaryotic expression vectors of pcDNA 3.1-PHD3 was constructed. HepG2 cells were transfected with recombinant plasmid pcDNA 3.1-PHD3 and empty vector plasmid pcDNA 3.1 by lipofectamine 2000 as transfected group, control group respectively, while the HepG2 cell without any operation was considered as parental group. Steady expression cells were gotten by G418 selecting. RT-PCR and agarose gel electrophoresis were used to confirm the expression of PHD3 in HepG2 cells and transfection successfully. The growth of these cells in vivo were also observed by injecting three groups of cell into nude mice, and volume were measured and compared. RESULTS: The recombinant plasmid pcDNA 3.1-PHD3 and empty vector plasmid pcDNA 3.1 were successfully transfected into human hepatoma HepG2 cell line and showed stable expression in this cell line. Tumors were observed in nude mice when the transfectant cells were xenografted successfully, The average tumor size of PCDNA (3.1)-PHD3 groups are significant different compared with other two groups (P < 0.001). CONCLUSION: The PHD3 gene may have negative influence of growth and proliferation on HepG2 cells in vitro. The PHD3 may be a potentially tumor suppressor.

Tumor suppressor TSLC1 inhibits growth, proliferation, invasiveness and angiogenesis in nude mice xenografted tumor of Eca109 cells.

Tumor suppressor in lung cancer 1 (TSLC1) is a novel tumor suppressor gene whose inactivation is implicated in the occurrence, invasion, metastasis and prognosis of esophageal cancer. TSLC1 was studied by comparing the tumor formation of TSLC1 transfectant and control cells in nude mice. Compared with blank group and mock group, tumor size and infiltrating range of transfected group was less, differentiation of tumor tissue was slightly better, and differences of tumor angiogenesis was worse. There was no obvious difference between blank group and mock group. We have shown TSLC1 gene inhibited the growth proliferation, infiltration and angiogenesis of Eca109 cells.

Function and expression of prolyl hydroxylase 3 in cancers.

Hypoxia inducible factor (HIF) is a product of tumor cells that plays an important role in protecting tumor cells and adjusting to low oxygen tension through driving the progression and aggressiveness of tumors and changing the growth, angiogenesis, differentiation and metastasis of tumors. Prolyl hydroxylase 3 (PHD3) is a member of PHDs that are induced in hypoxia. Many studies have shown that PHD3 not only can hydroxylate HIF-1α, but also has various other biological functions. Thus PHD3 plays significant roles in suppressing the growth, angiogenesis, differentiation and metastasis of tumors and promoting apoptosis of tumors under hypoxic conditions. It may become a new tumor suppressor gene and also may become a new approach to investigate tumors.

Construction of a recombinant eukaryotic expression vector containing PHD3 gene and its expression in HepG2 cells.

Prolyl hydroxylase domain 3 (PHD3) is a hypoxia inducible factor-α (HIFα) regulator; it degrades HIFα in the presence of oxygen. Recently, there have been an increasing number of studies about the role of PHD3 in proliferation and apoptosis of cancer cells. However, most of the evidence for the role of PHD3 is observational, and little is known of the molecular mechanism. In our current study, we constructed a recombinant eukaryotic expression vector containing the PHD3 gene and detected its biological activity in human hepatoma cell line (HepG2 cells). We successfully constructed a recombinant pcDNA 3.1(+)-PHD3 plasmid; the results showed that PHD3 overexpression could inhibit the proliferation of HepG2 cells and induce apoptosis by activating caspase-3 activity. Our study has provided preliminary materials and data for further investigation of the effect of PHD3 on HepG2 cells.