Histology and histopathology Vol.36, nº3 (2021)
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- PublicationOpen AccessFrequent DYRK2 gene amplification in micropapillary element of lung adenocarcinoma - an implication in progression in EGFR-mutated lung adenocarcinoma(Universidad de Murcia, Departamento de Biologia Celular e Histiologia, 2021) Koike, Chihiro; Okudela, Koji; Matsumura, Mai; Mitsui, Hideaki; Suzuki, Takehisa; Arai, Hiromasa; Kataoka, Toshiaki; Ishikawa, Yoshihiro; Umeda, Shigeaki; Tateishi, Yoko; Ohashi, KenichiThe present study aimed to discern the molecular alterations involved in the progression of EGFR-mutated lung adenocarcinoma (LADC). We previously demonstrated that the micropapillary (mPAP) element is the most important histological factor for assessing malignant grades in LADCs. Therefore, mPAP and other elements were separately collected from three cases of EGFR-mutated LADC using laser capture microdissection and subjected to a comprehensive mRNA expression analysis. We focused on DYRK2 in this study because its level showed a substantial increase in EGFR-mutated LADCs with mPAP. We also immunohistochemically examined 130 tumors for the expression of DYRK2. The results confirmed a strong expression of DYRK2 in EGFR-mutated LADC with mPAP. Fluorescent in situ hybridization (FISH) analyses targeting the DYRK2 locus revealed frequent gene amplification in EGFR-mutated LADC, specifically occurring in the high-grade components, like mPAP. In summary, the results of this study suggest that DYRK2 overexpression through gene amplification is one of the molecular mechanisms responsible for promoting the progression of EGFR-mutated LADC.
- PublicationOpen AccessThe pathogenesis and pathology of idiopathic pleuroparenchymal fibroelastosis(2021) Kinoshita, Yoshiaki; Ishii, Hiroshi; Nabeshima, Kazuki; Watanabe, KentaroIdiopathic pleuroparenchymal fibroelastosis (IPPFE) is a rare subtype of idiopathic interstitial pneumonias that consists of elastofibrosis involving the lung parenchyma and pleural collagenous fibrosis predominantly located in the upper lobes. IPPFE has various distinct clinical and physiological characteristics, including platythorax and a marked decrease of forced vital capacity with an increased residual volume on a respiratory function test. The concept of IPPFE is now widely recognized and some diagnostic criteria have been proposed. In addition, the accumulation of cases has revealed the pathological features of IPPFE. However, little is known about the pathogenesis or the process of disease formation in IPPFE. This review article will provide a summary of the pathological features and previously reported hypotheses on disease formation in IPPFE, to discuss the potential etiologies and pathogenesis of IPPFE.
- PublicationOpen AccessShufeng Jiedu capsules protect rats against LPS-induced acute lung injury via activating NRF2-associated antioxidant pathway(Universidad de Murcia, Departamento de Biologia Celular e Histiologia, 2021) Liao, Qingwu; Chen, Wenan; Tong, Zhufeng; Xue, Mingming; Gu, Tianwen; Yuan, Ying; Song, Zhenju; Tao, ZhengangShufeng Jiedu capsule (SFJDC) is a traditional Chinese medicine, which has been used for the treatment of respiratory infections for more than thirty years in Hunan (China). SFJDC protected rats against LPS-induced acute lung injury (ALI); however, the molecular mechanisms underlying the therapeutic effects of SFJDC remain unclear. Therefore, this study aimed at analyzing the major anti-inflammatory compounds of SFJDC and exploring the underlying molecular mechanisms. SFJDC dissolved in water was fingerprinted by UPLC/Q-TOF. Inflammation response was assessed by histopathological examination and ELISA assay. Arterial blood gases were also analyzed to evaluate the function of rat lungs. The expression levels of Kelch-like ECH-associating protein 1 (Keap1), Nrf2, heme oxygenase-1 (HO1), Cullin 3 (CUL3) and NQO1 were analyzed by Western blotting. Results indicated that SFJDC alleviated inflammation response by reducing the level of inflammatory cytokines, and upregulation of glutathione-S-transferase (GST) and superoxide dismutase (SOD) in lung tissues. Furthermore, SFJDC suppressed LPS-induced upregulation of Keap 1 and CUL3 in rat lungs. The expression of NRF2 HO1 and NQO1 were further upregulated by SFJDC in the presence of LPS, indicating that SFJDC might activate the NRF2- associated antioxidant pathway. In conclusion, SFJDC treatment may protect the rat lungs from LPS by alleviating the inflammation response via NRF2- associated antioxidant pathway
- PublicationOpen AccessMiR-590-5p regulates cell proliferation, apoptosis, migration and invasion in oral squamous cell carcinoma by targeting RECK(Universidad de Murcia, Departamento de Biologia Celular e Histiologia, 2021) Bao, Wei-Wei; Shi, You-Ling; Ma, Yan; Qu, Xing-Hui; Pang, Guang-Ming; Yang, LeiObjective. To discover the role of miR-590- 5p in oral squamous cell carcinoma (OSCC) progression and the corresponding mechanism via the targeting RECK. Methods. OSCC (n=85) and normal oral tissues (n=60) were collected to quantify the miR-590-5p expression by using qRT-PCR. Then SCC-15 and OECM1 cells were selected and divided into Mock, inhibitor NC, miR-590-5p inhibitor, si-RECK and miR-590-5p inhibitor + si-RECK groups. Dual-luciferase reporter gene assay was used to verify if miR-590-5p could target RECK. The biological behaviors of OSCC cells were evaluated by MTT, Wound-healing, Transwell and Flow cytometry. The expression of miR-590-5p and RECK was measured by qRT-PCR and Western blotting, respectively. Results. Overexpression of miR-590-5p was found in OSCC tissues. The expression of miR-590-5p was significantly associated with the clinical TNM stage, differentiation degree, and lymph node metastasis of OSCC. RECK was identified as a direct target of miR590-5p. Compared with the Mock group, cells in the miR-590-5p inhibitor group were decreased in terms of proliferation, invasion, and migration, and increased in cell apoptosis, accompanied by down-regulated miR590-5p, Bcl-2/Bax and MMP-9, and up-regulated RECK. By contrast, si-RECK group presented completely opposite changes, and si-RECK reversed the inhibitory effect of miR-590-5p inhibitor on the OSCC cell growth. Conclusion. MiR-590-5p expression was obviously increased in OSCC, and inhibiting miR-590-5p enhanced the expression of its target gene RECK, thereby suppressing proliferation, migration and invasion of OSCC cells and promoting apoptosis of OSCC cells
- PublicationOpen AccessImplications of androgen receptor and FUS expression on tumor progression in urothelial carcinoma(Universidad de Murcia, Departamento de Biologia Celular e Histiologia, 2021) Abd Raboh, Nermine Mohamed; Adel Hakim, Sarah; Abd El Atti, Rasha MohamedAndrogen receptor (AR) interact with many pathways involved in bladder cancer development and progression. FUS (fused in liposarcoma), a multifunctional protein essential for different cellular processes, has been demonstrated as a key link between androgen receptor signaling and cell-cycle progression in prostate cancer but has not been examined in urothelial carcinoma (UC) despite an intimate association between prostate and bladder carcinogenesis. Aim. to examine the immunohistochemical expression of AR and FUS in urothelial carcinoma in relation to prognostic parameters and to extrapolate any possible link between the expression of both markers and tumor progression. Study design. Retrospective study using immunohistochemical staining for AR and FUS on (88) cases of urothelial carcinoma. Results. AR shows statistically significant relations with late tumor stage, high tumor grade, and nonpapillary tumor pattern. On the other hand, FUS expression correlates with early tumor stage, low tumor grade and papillary pattern. An inverse relation is found between AR and FUS expression (p=0.001). Cases with high AR IHC expression show statistically significant shorter OS, RFS and PFS compared to cases with low AR expression. Cases with high FUS IHC expression reveal statistically significant longer OS, RFS and PFS compared to cases with low FUS expression. Conclusion. FUS expression is associated with favorable prognostic parameters of UC. A possible interaction is suggested between FUS and AR pathways involved in urothelial cancer progression. Manipulating FUS levels and androgen deprivation therapy can provide new promising targets for treatment trials.