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1.
Medicine (Baltimore) ; 101(26): e29341, 2022 Jul 01.
Article in English | MEDLINE | ID: mdl-35777039

ABSTRACT

INTRODUCTION: Reports on the coexistence of epithelioid angiosarcoma (EA) and papillary thyroid carcinoma (PTC) are rare. Over the past 50 years, only 2 cases of coexistence of EA and PTC have been reported in English literature. Therefore, we report a rare case of coexistence of EA and PTC treated with surgery and adjuvant radiation therapy. PATIENT CONCERNS: A 64-year-old man visited our hospital with a painless mass in the left submandibular gland, with poor mobility. DIAGNOSIS: Neck ultrasonography revealed nodules in the left submandibular gland and multiple cystic-solid mixed nodules in the left thyroid gland. Pathological findings revealed coexistence of EA in the left submandibular gland area and PTC in the left thyroid gland. INTERVENTIONS: The patient underwent resection of the left submandibular gland, deep maxillofacial tumor, total thyroidectomy, left neck I, II, III, and VI regional lymph node dissection, and recurrent laryngeal nerve exploration under general anesthesia. Two months postoperatively, the patient also received adjuvant radiation therapy in the local and adjacent areas, with 4MV-X IMRT DT50GY at 2Gy/day 25 fractions. OUTCOMES: The follow-up period was 37 months. The patient recovered well without focal neurological deficits, local recurrence, or distant metastasis after surgery, except for grade I skin reaction after adjuvant radiation therapy. CONCLUSIONS: This is a rare case report of the coexistence of EA in the left submandibular gland and PTC in the left thyroid gland. Although multiple examinations were used, precise preoperative diagnosis was challenging owing to the coexistence of EA and PTC. Surgery and radiotherapy were effective treatments for the coexistence of EA and PTC in this case.


Subject(s)
Hemangioendothelioma, Epithelioid , Hemangiosarcoma , Thyroid Neoplasms , Hemangiosarcoma/complications , Hemangiosarcoma/diagnosis , Hemangiosarcoma/surgery , Humans , Male , Middle Aged , Neck , Submandibular Gland , Thyroid Cancer, Papillary/complications , Thyroid Neoplasms/complications , Thyroid Neoplasms/diagnosis , Thyroid Neoplasms/surgery
2.
Dis Markers ; 2021: 8897906, 2021.
Article in English | MEDLINE | ID: mdl-33564344

ABSTRACT

BACKGROUND: Long intergenic noncoding RNA1184 (linc01184) has been recently discovered; however, its role in human diseases is limited to date. The present study is aimed at investigating the expression pattern and mechanism of linc01184 in colorectal cancer (CRC) tumorigenesis. METHODS: The expression of linc01184 in CRC tissues and cell lines was compared with that in normal controls. The functions of linc01184 in CRC cells were identified by overexpression and small interfering RNA (siRNA) approaches in vitro. Meanwhile, the target gene prediction software, luciferase reporter, RNA pull-down, and western blotting assays were used to analyze the oncogenic mechanism. RESULTS: We found that linc01184 was obviously upregulated in CRC tissues and cells when compared to normal controls, and its upregulation had a positive association with the CRC progression. linc01184 knockdown significantly suppressed CRC cell proliferation and invasion and promoted apoptosis. Besides, linc01184 acted as a competitive endogenous RNA (ceRNA) by directly binding to microRNA-331 (miR-331), and its overexpression resulted in notable increases of human epidermal growth factor receptor 2 (HER2), phosphorylated Ser/Thr kinases (p-Akt), and extracellular regulated protein kinase 1/2 (p-ERK1/2) at posttranscriptional levels in CRC cells, which were antagonized by miR-331. CONCLUSIONS: The findings reveal for the first time that linc01184 is an enhancer for the proliferation and invasion of CRC by functioning as a ceRNA through the linc01184-miR-331-HER2-p-Akt/ERK1/2 pathway regulatory network.


Subject(s)
Biomarkers, Tumor/genetics , Colorectal Neoplasms/genetics , RNA, Long Noncoding/genetics , Aged , Biomarkers, Tumor/metabolism , Caco-2 Cells , Colorectal Neoplasms/metabolism , Colorectal Neoplasms/pathology , Female , Gene Expression Regulation, Neoplastic , HCT116 Cells , HT29 Cells , Humans , Male , MicroRNAs/genetics , MicroRNAs/metabolism , Middle Aged , Mitogen-Activated Protein Kinase 1/genetics , Mitogen-Activated Protein Kinase 1/metabolism , Mitogen-Activated Protein Kinase 3/genetics , Mitogen-Activated Protein Kinase 3/metabolism , Proto-Oncogene Proteins c-akt/genetics , Proto-Oncogene Proteins c-akt/metabolism , RNA, Long Noncoding/metabolism , Receptor, ErbB-2/genetics , Receptor, ErbB-2/metabolism , Up-Regulation
3.
Oncotarget ; 8(17): 28135-28143, 2017 Apr 25.
Article in English | MEDLINE | ID: mdl-28427236

ABSTRACT

Many studies have reported an association between the glutathione S-transferase M1 null and T1 null polymorphisms and lung cancer risk. However, the combined effects of GSTM1 null and GSTT1 null polymorphisms have not been reported previously. We, therefore, performed a meta-analysis to investigate the combined effects. 40 publications with 44 case-control studies were selected in the meta-analysis, including 13,706 cases and 13,093 controls. Significant association was observed between the combined effects of GSTM1 and GSTT1 polymorphisms and lung cancer risk when all the eligible studies were pooled into the meta-analysis. When we performed subgroup analysis, significantly increased lung cancer risk was observed in Caucasians (- - vs. + + : OR = 1.23, 95% CI: 1.07 to 1.41), Asians (- - vs.- +: OR = 1.24, 95% CI: 1.10 to 1.41; recessive model: OR = 1.45, 95% CI: 1.19 to 1.77; dominant model: OR = 1.53, 95% CI: 1.24 to 1.90), Indians (- - vs. + + : OR = 2.53, 95% CI: 1.61 to 3.98; recessive model: OR = 1.69, 95% CI: 1.07 to 2.67; dominant model: OR = 2.11, 95% CI: 1.36 to 3.28), hospital-based studies, and population-based studies. In summary, this meta-analysis indicates that the combined effects of the GSTM1 and GSTT1 polymorphisms are associated with increased lung cancer risk in Asians, Caucasians, and Indians.


Subject(s)
Genetic Association Studies , Genetic Predisposition to Disease , Glutathione Transferase/genetics , Lung Neoplasms/genetics , Polymorphism, Genetic , Alleles , Asian People , Case-Control Studies , Genotype , Humans , Odds Ratio , Polymorphism, Single Nucleotide , Publication Bias , White People
4.
Oncol Lett ; 12(3): 2045-2047, 2016 Sep.
Article in English | MEDLINE | ID: mdl-27602136

ABSTRACT

Leiomyomas in the female reproductive system are commonly located in the uterus and typically regress following the menopause. Vulval leiomyomas are rare, and to the best of our knowledge, perineal leiomyomas in postmenopausal women have not been previously reported in the literature. The present case describes a 60-year-old Chinese woman who experienced perineal tenderness and lumbosacral radiating pain. The patient, who went through the menopause 12 years previously, had presented with a painful perineal mass for 1 year, which was subsequently diagnosed as a postmenopausal perineal leiomyoma. The mass was locally resected, and histopathological examination of the lesion resulted in a diagnosis of benign epithelioid leiomyoma. Immunohistochemical staining identified that the leiomyoma was positive for estrogen receptor and negative for progesterone receptor expression. The patient was followed up for 1 year and did not experience any pain or recurrence. The symptoms of local and lumbosacral radiating pain are extremely rare and may be induced by peripheral nerve stimulation. The etiology of postmenopausal perineal leiomyoma may be associated with infection, dietary, stress and environmental factors, and the role of estrogen cannot be overemphasized in cases of postmenopausal leiomyoma.

5.
Oncotarget ; 7(11): 12393-403, 2016 Mar 15.
Article in English | MEDLINE | ID: mdl-26848622

ABSTRACT

Renal cell carcinoma (RCC) is one of the common tumors in the urinary system without effective therapies. Angiomotin (Amot) can interact with Yes-associated protein (YAP) to either stimulate or inhibit YAP activity, playing a potential role in cell proliferation. However, the role of Amot in regulating the proliferation of renal epithelial and RCC cells is unknown. Here, we show that Amot is expressed predominantly in the nucleus of RCC cells and tissues, and in the cytoplasm and nucleus of renal epithelial cells and paracancerous tissues. Furthermore, Amot silencing inhibited proliferation of HK-2 and 786-O cells while Amot upregulation promoted proliferation of ACHN cells. Interestingly, the location of Amot and YAP in RCC clinical samples and cells was similar. Amot interacted with YAP in HK-2 and 786-O cells, particularly in the nucleus. Moreover, Amot silencing mitigated the levels of nuclear YAP in HK-2 and 786-O cells and reduced YAP-related CTGF and Cyr61 expression in 786-O cells. Amot upregulation slightly increased the nuclear YAP and YAP-related gene expression in ACHN cells. Finally, enhanced YAP expression restored proliferation of Amot-silencing 786-O cells. Together, these data indicate that Amot is crucial for the maintenance of nuclear YAP to promote renal epithelial and RCC proliferation.


Subject(s)
Carcinoma, Renal Cell/metabolism , Carcinoma, Renal Cell/pathology , Intercellular Signaling Peptides and Proteins/metabolism , Kidney Neoplasms/metabolism , Kidney Neoplasms/pathology , Membrane Proteins/metabolism , Nuclear Proteins/metabolism , Transcription Factors/metabolism , Angiomotins , Cell Cycle Proteins , Cell Line, Tumor , Cell Nucleus/metabolism , Cell Proliferation/physiology , Epithelial Cells/metabolism , HEK293 Cells , Humans , Kidney Tubules/cytology , Kidney Tubules/metabolism , Microfilament Proteins , Transfection
6.
Int J Clin Exp Pathol ; 8(8): 9647-54, 2015.
Article in English | MEDLINE | ID: mdl-26464732

ABSTRACT

Metastases to the breast from extramammary malignancies are extremely rare. Ruling out the diagnosis of primary breast tumor is important in order to decide on clinical management and predict prognosis. We report a case of metastasis to the breast from a pulmonary adenocarcinoma, with extensive micropapillary component, diagnosed concomitantly with the primary tumor. A 52 year-old female patient presented with mammary gland tingling and dyspnea accompanied with fatigued of 4 months duration and a nodular shadows in the front of the upper lobe was found on a chest computed tomography (CT) scan. The original clinical diagnosis was right breast cancer with lung and bone metastasis, or breast and lung double primary cancers. In addition,on physical examination a poorly defined mass was noted in the upper outer quadrant of the right breast. The patient underwent thoracocentesis and breast biopsy. By imageology, cytology, histology and immunohistochemistry, we diagnosed primary lung cancer with metastases to the right breast and bone. The metastatic anatomic sites demonstrated histologically extensive micropapillary component, which is recently recognized as an important prognostic factor. The patient was administered 4 cycles of cisplatin and docetaxel, although no clinical response was seen, the patient is still alive 9 months after diagnosis. The result of immunohistochemistry is a useful supplement in differential diagnosis.


Subject(s)
Adenocarcinoma/secondary , Breast Neoplasms/secondary , Lung Neoplasms/pathology , Biomarkers, Tumor/analysis , Female , Humans , Immunohistochemistry , Middle Aged
7.
World J Gastroenterol ; 18(17): 2053-60, 2012 May 07.
Article in English | MEDLINE | ID: mdl-22563192

ABSTRACT

AIM: To develop an affinity peptide that binds to gastric cancer used for the detection of early gastric cancer. METHODS: A peptide screen was performed by biopanning the PhD-12 phage display library, clearing non-specific binders against tumor-adjacent normal appearing gastric mucosa and obtaining selective binding against freshly harvested gastric cancer tissues. Tumor-targeted binding of selected peptides was confirmed by bound phage counts, enzyme-linked immunosorbent assay, competitive inhibition, fluorescence microscopy and semi-quantitative analysis on immunohistochemistry using different types of cancer tissues. RESULTS: Approximately 92.8% of the non-specific phage clones were subtracted from the original phage library after two rounds of biopanning against normal- appearing gastric mucosa. After the third round of positive screening, the peptide sequence AADNAKTKSFPV (AAD) appeared in 25% (12/48) of the analyzed phages. For the control peptide, these values were 6.8 ± 2.3, 5.1 ± 1.7, 3.5 ± 2.1, 4.6 ± 1.9 and 1.1 ± 0.5, respectively. The values for AAD peptide were statistically significant (P < 0.01) for gastric cancer as compared with other histological classifications and control peptide. CONCLUSION: A novel peptide is discovered to have a specific binding activity to gastric cancer, and can be used to distinguish neoplastic from normal gastric mucosa, demonstrating the potential for early cancer detection on endoscopy.


Subject(s)
Peptide Library , Peptides/analysis , Stomach Neoplasms/chemistry , Stomach Neoplasms/diagnosis , Binding, Competitive , Biopsy , Cell Line, Tumor , Early Detection of Cancer , Enzyme-Linked Immunosorbent Assay , Humans , Immunohistochemistry
8.
Xi Bao Yu Fen Zi Mian Yi Xue Za Zhi ; 28(4): 371-3, 2012 Apr.
Article in Chinese | MEDLINE | ID: mdl-22482406

ABSTRACT

AIM: To study the changes of the cell growth, cell cycle distribution and cell apoptosis of colon cancer cell, HT-29, when C-erbB2 gene was knockdown by shRNA against C-erbB2. METHODS: Cell growth, cell cycle distribution and cell apoptosis were compared among three groups including plasmid experimental group(PEG), transfected reagent control group(TRCG)and negative plasmid control group(NPCG). Cell growth was measured by MTT assay. Cell cycle distribution and cell apoptosis were detected by flow cytometry. RESULTS: The inhibition rate of cell growth of PEG, TRCG and NPCG were 39.65%, 7.23% and 8.05% respectively. The cell growth was significantly inhibited in PEG(P<0.01). The cells of G0/G1 phase were 74.93%, 67.19%, 68.05% respectively in PEG, TRCG and NPCG. The cells of G0/G1 phase in PEG were significantly more than those in TRCG and NPCG(P<0.05).While the cells of S phase were 7.81%, 14.02%, 13.70% in PEG, TRCG and NPCG respectively. The cells of S phase in PEG were significantly less than those in TRCG or NPCG(P<0.05).The cell apoptosis rate were 19.21%, 3.13%, 4.08% in PEG, TRCG and NPCG respectively. The cell apoptosis rate in PEG was significantly higher than those in TRCG or NPCG(P<0.01). CONCLUSION: Cell growth was inhibited by shRNA against C-erbB2 gene. Cell cycle was blocked in G0/G1 phase and apoptosis was induced by C-erbB2 shRNA. This indicates C-erbB2 gene plays important roles in the carcinogenesis and development of colon cancer.


Subject(s)
Apoptosis/genetics , Cell Cycle/genetics , Cell Proliferation , RNA, Small Interfering/genetics , Receptor, ErbB-2/genetics , Apoptosis/physiology , Cell Cycle/physiology , Cell Cycle Checkpoints/genetics , Cell Cycle Checkpoints/physiology , Cell Survival/genetics , Cell Survival/physiology , Colonic Neoplasms/genetics , Colonic Neoplasms/metabolism , Colonic Neoplasms/pathology , Flow Cytometry , HT29 Cells , Humans , Plasmids/genetics , RNA Interference , Receptor, ErbB-2/metabolism , Time Factors , Transfection
9.
Mol Med Rep ; 5(3): 866-72, 2012 03.
Article in English | MEDLINE | ID: mdl-22200761

ABSTRACT

This study aimed to investigate the involvement of c-erbB-2, encoded by the receptor tyrosine kinase ERBB2 gene, in the pathogenesis of colorectal cancer and to validate its potential as an anticancer target. Immunohistochemical and histopathological analyses were applied in tissue samples derived from 80 colorectal cancer patients. ERBB2 stable small hairpin RNA (shRNA) knockdown in HT29 human colorectal cancer cells was confirmed by RT-PCR and western blotting. Cell cycle profile and apoptosis were measured using PI or Annexin V-PI dual staining. A significant correlation between ERBB2 levels and Dukes' stage of colorectal cancer, in both the primary malignancy and lymph node metastatic tissues, was observed. ERBB2-depleted HT-29 cells exhibited increased sensitivity to radiation compared to control cells, likely due to enhanced G0/G1 phase cell cycle arrest and apoptosis. ERBB2 may be involved in the malignancy and metastasis of colorectal cancer. Overexpressed ERBB2 may constitute a potential target for colorectal cancer therapy.


Subject(s)
Colorectal Neoplasms/pathology , RNA Interference , Radiation Tolerance/genetics , Receptor, ErbB-2/genetics , Adult , Aged , Apoptosis/radiation effects , Cell Line, Tumor , Colorectal Neoplasms/metabolism , Female , G1 Phase Cell Cycle Checkpoints/radiation effects , Gene Knockdown Techniques , Humans , Immunohistochemistry , Lymphatic Metastasis , Male , Middle Aged , Neoplasm Staging , RNA, Small Interfering/metabolism , Receptor, ErbB-2/antagonists & inhibitors , Receptor, ErbB-2/metabolism
10.
Nan Fang Yi Ke Da Xue Xue Bao ; 29(9): 1870-3, 2009 Sep.
Article in Chinese | MEDLINE | ID: mdl-19778814

ABSTRACT

OBJECTIVE: To construct a plasmid carrying small interfering RNA (siRNA) targeting human C-erbB2 gene (pGenesil- erbB2) and test its effect on Her-2 expression at the post-transcriptional level in human colon cancer cell lines HT-29 cells that highly express erbB2. METHODS: A HT-29 cell line that highly expressed CerbB-2 was selected using immunohistochemical method. The double-stranded siRNA targeting human CerbB-2 cDNA and the negative control fragment were cloned into pGenesil-1 vector, and after identification and sequence analysis, the constructed pGenesil-erbB2 plasmid was transfected into the selected HT-29 cell line. RESULTS: The pGenesil-erbB2 plasmid was successfully constructed and stably transferred into HT-29 cells. The transfection resulted in significant inhibition of Her-2 protein expression in the HT-29 cells, as shown by Western blotting. CONCLUSION: The pGenesil-erbB plasmid we constructed can be stably transfected into HT-29 cells to inhibit the expression of Her-2 protein, and can be useful in further studies of increasing the radiosensitivity of HT-29 cell lines.


Subject(s)
Genes, erbB-2/genetics , Plasmids/genetics , RNA, Small Interfering , Receptor, ErbB-2/biosynthesis , Base Sequence , HT29 Cells , Humans , Molecular Sequence Data , RNA Interference , Receptor, ErbB-2/genetics , Transfection
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