Acta Universitatis Medicinalis Anhui

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Anhui Provincial Education Department

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Anhui Medical University

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Weng Jianping

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Molecular mechanisms and clinical therapeutic advances in lung cancer liver metastasis

Ji Pengcheng1 , 2 , Ye Yuanzi3 , Shao Changchun1

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Spatial and temporal epidemiological characteristics of tuberculosis in Shache County , Kashgar Region , 2019—2021

Chen Xiaodie1 , Maiwulajiang Yimamu2 , Chang Minli 1 , Zhang Liping3 , Zheng Yanling3

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abstract:
To investigate the characteristics of temporal and spatial distribution of tuberculosis epidem- ics in Shache County , Kashgar Region , Xinjiang. Methods Information on the incidence of tuberculosis in Sacha County from 2019—2021 was collected and spatiotemporally analyzed by applying the circular distribution method , local spatial autocorrelation analysis , hot and cold spot analysis , directional distribution and spatial center of gravity methods . Results The total number of tuberculosis cases in Shache County in 2019—2021 was 8 , 345 , of which 52. 03% were male and 47. 97% were female , and the patients were predominantly 60 - 75 years old . The number of reported incidences of TB in Tagarqi Township , Shache Township , and Chajek Township ranked among the top three in the county . Spring and summer were the disease-prone seasons for TB , and mid-March to mid-July was the period of high disease incidence . Misha Township and Ishkuli Township are the “high and high ”gathering areas , while the “low and low ”gathering areas are mainly concentrated in Khoshrav Township and Karasu Township . The hotspots of TB incidence in Shache County were Tagarqi Township , Misha Township , and Ishkuli Township . During the study period , the center of gravity of TB incidence in shache county of kashgar area gradually shifted from the southwest to the northeast. Conclusion In Shache County , there is a certain degree of aggregation of tuberculosis outbreaks , with more men than women reporting illnesses , a larger proportion of older people , and a strong seasonal incidence of the disease , with Mixia Township and Ishikuli Township being the key areas of incidence . Relevant departments should continue to strengthen the disease surveillance of key populations and regions during the high incidence of tuberculosis , and take appropriate intervention measures to reduce the risk of tuberculosis transmis- sion .

Expression of PHB2 in breast cancer and its effect on proliferation , migration , and invasion

Pei Yating1 , Shen Yuting1 , Wang Juqin1 , Luo Wenwu2 , Guo Qianying2 , Wu Zhengsheng1 , 2

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abstract:
To explore the expression of prohibitin2 (PHB2) in breast cancer and its effect on the bio- logical behaviors of tumor cells . Methods Immunohistochemistry was used to detect the expression of PHB2 pro- tein in breast cancer tissues and its relationship with clinicopathologic features . Breast cancer stable transient cell lines were constructed with knockdown and overexpression of PHB2 , respectively. The effects of PHB2 on cell pro- liferation , migration and invasion ability were detected by clone formation assay , scratch assay and Transwell assay. Western blot (WB) was used to detect the effects of PHB2 on the expression of epithelial-mesenchymal transition (EMT) - related markers , including E-cadherin , N-cadherin , Snail family transcriptional repressor 1 (Snail) pro- tein , Vimentin , and Claudin-1 . The effect of PHB2 on tumorigenicity in vivo was detected by subcutaneous tumor formation assay in nude mice . Results The result of immunohistochemical showed that PHB2 was highly expressed in breast cancer and the expression of PHB2 was significantly positive correlated with tumor size , human epidermal growth factor receptor-2 (HER-2) status and proliferation index Ki-67 levels (P < 0. 05) . Clone formation assay , scratch assay and Transwell assay revealed that knockdown of significantly inhibited the proliferation , migration and invasion ability of breast cancer cells ( P < 0. 01) , while the overexpression of PHB2 significantly promoted cell proliferation , migration and invasion (P < 0. 01) . The result of subcutaneous tumor formation experiment in nude mice revealed a significant decrease in tumor volume and weight in knockdown PHB2 mice (P < 0. 000 1) , while PHB2 overexpression tumors significantly increased in volume and weight (P < 0. 001) . WB assay showed that the protein expression of epithelial marker E-cadherin increased , while the expressions of mesenchymal markers N-cad- herin , Snail and Vimentin decreased significantly after PHB2 knockdown with them in control cells (P < 0. 01) . The expression of Claudin-1 decreased , while the expressions of N-cadherin , Snail and Vimentin increased signifi- cantly in PHB2 overexpression cells (P < 0. 05) . Conclusion PHB2 is highly expressed in breast cancer and pro- motes multiple malignant biological behaviors in tumor cells , suggesting PHB2 may be a potential target for breast cancer diagnosis and treatment.

KRT14 promotes the invasion and migration of basal-like breast cancer through activating the Wnt/β-catenin pathway

Cheng Zheng1 , Zhang Manman1 , Zhou Jingni2 , Guo Qianying1 , 2 , Wu Zhengsheng1 , 2

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abstract:
To investigate the expression of Keratin 14 (KRT14) in Basal-like Breast Cancer (BLBC) and its biological functions and mechanisms . Methods The expression levels of KRT14 mRNA in BLBC and para- cancer breast tissues were analyzed using The Cancer Genome Atlas ( TCGA) database . qPCR , Western blot (WB) , and immunohistochemistry were employed to detect KRT14 expression in BLBC and adjacent normal tis- sues , and its correlation with clinicopathological features was analyzed . KRT14 overexpression and knockdown were performed in breast cancer cells , and cell scratch and transwell assays were performed to evaluate changes in migra- tion and invasion abilities . To investigate the expression of proteins related to the Wnt/β-catenin signaling pathway , including β-catenin ( catenin Beta 1) , Wnt1 ( wingless-type MMTV integration site family , member 1) , MMP7 ( matrix metallopeptidase 7) , and c-Myc (cellular myelocytomatosis viral oncogene homolog) , as well as the cellu- lar localization of β-catenin , WB and immunofluorescence (IF) techniques were employed . Additionally , a Wnt/ β-catenin signaling pathway inhibitor was used to verify the mechanism of action of KRT14 . Results The expres- sion of KRT14 was significantly higher in BLBC tissues compared to normal tissues (P < 0. 05) , and was associated with higher T stage , and histological grade( P < 0. 05) . The overexpression of KRT14 significantly enhanced the migration and invasion abilities of breast cancer cells , while the knockdown of KRT14 significantly reduced those a- bilities (P < 0. 01) . The overexpression of KRT14 can increase the expression levels of Wnt/β-catenin pathway-re- lated proteins β-catenin , Wnt1 , MMP7 , and c-Myc , thereby activating the Wnt/β-catenin pathway . Moreover , the inhibition of this pathway can eliminate the effects of KRT14 on cell migration and invasion . Conclusion The high expression of KRT14 in BLBC may promote the migration and invasion of breast cancer cells through the Wnt/β- catenin signaling pathway .

Exploration of the role of ABCG5 inhead and neck squamous cell carcinoma

Wu Xiangping1 , Wang Yan2 , Yao Changyu 1

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abstract:
To investigate the regulatory role of ABCG5 in head and neck squamous cell carcinoma. Methods Immunohistochemical staining was used to detect the expression of ABCG5 in 105 patients with hypopha- ryngeal carcinoma , and the relationship between the expression and the long-term survival time of the patients was analyzed . Immunowestern blotting and flow cytometry were used to detect the expression of ABCG5 in head and neck squamous cell carcinoma cell lines . Flow sorting was employed to investigate the differences in proliferation and metastasis , spheroidization ability , and expression of stem cell molecules between ABCG5 positive and negative cells . si RNA interference was used to further demonstrate whether ABCG5 affects the malignant phenotype . Re- sults ABCG5 was associated with poor prognosis in patients with hypopharyngeal carcinoma. ABCG5 was enriched in stem cells of head and neck squamous cell carcinoma. ABCG5-positive cells had stronger proliferation ( P < 0. 001), metastasis (P < 0. 01), and spheroid formation abilities (P < 0. 001) than negative cells . The expression levels of some stem cell molecules (SOX2 、NANOG、SOX9 、OCT4 、CD44) in ABCG5-positive cells were higher than those in ABCG5-negative cells . The expression of epithelial cell protein E-cadherin was lower in ABCG5-positive cells than that in ABCG5-negative cells , and the expression of interstitial cell proteins N-cadherin , Slug , Snail 1 , and Vimentin were higher (P < 0. 01) . Moreover , interfering with ABCG5 expression significantly inhibited tumor cell spheroid formation (P < 0. 001), as well as the expression of proteins related to cancer stem cells and epitheli- al-mesenchymal transition . Conclusion ABCG5 has a potential biological role in maintaining the function of head and neck squamous cell carcinoma stem cells .

Bortezomib inhibits the malignant biological behaviors of pancreatic cancer cells and liver metastasis

Chen Yinfeng1 , Huang Xing1 , 2

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abstract:
To investigate the potential of bortezomib in inhibiting the malignant biological behaviors and liver metastasis of pancreatic cancer cells . Methods KPC and Panc02 cell lines were used as a couple of working cells in this study . The CCK-8 assay was used to assess the effect of bortezomib on cell viability in murine pancreatic cancer cells , and the half inhibitory concentration ( IC50 ) values were calculated . The EdU assay was performed to evaluate the impact of bortezomib on the proliferation of these two cell lines . Apoptosis assays were conducted to investigate the pro-apoptotic effects of bortezomib on pancreatic cancer cells . Colony formation , scratch wound healing , and Transwell assays were used to examine the effects of bortezomib on the proliferation , migration , and invasion of pancreatic cancer cells . QRT-PCR and Western blot were employed to assess the impact of bortezomib on the expression of epithelial-mesenchymal transition ( EMT) related markers , including Cdh1 , Cdh2 , Vim and Snail gene and E-cadherin protein , N-cadherin protein , Vimentin protein and Snail protein . An in vivo spleen-to-liver metastasis model was established to evaluate the therapeutic value of bortezomib in inhibiting pancreatic cancer liver metastasis . Results The CCK-8 assay showed that bortezomib significantly reduced the via- bility of KPC and Panc02 cells (P < 0. 000 1) , with IC50 values of approximately 118. 70 nmol/L and 34. 16 nmol/ L , respectively . The EdU assay showed that bortezomib markedly inhibited the proliferative capacity of pancreatic cancer cells (P < 0. 01) . Apoptosis assays showed that bortezomib promoted both early and late apoptosis in pan- creatic cancer cells (P < 0. 05) . Colony formation , scratch wound healing , and Transwell assays showed that bort- ezomib effectively suppressed colony formation ( P < 0. 01) , migration , and invasion ( P < 0. 01) of pancreatic cancer cells . qRT-PCR and Western blot analyses showed that bortezomib altered the expression of EMT-related markers at both the mRNA ( the expression level of Cdh1 gene increased , while the expression levels of Cdh2 , Vim and Snail genes decreased . ) ( P < 0. 000 1) and protein ( the expression level of E-cadherin protein increased , while the expression levels of N-cadherin protein , Vimentin protein and Snail protein decreased) levels in pancreat- ic cancer cells . The in vivo spleen-to-liver metastasis model demonstrated that bortezomib significantly inhibited pancreatic cancer liver metastasis ( P < 0. 01) . Conclusion Bortezomib can inhibit the malignant biological be- haviors of pancreatic cancer cells , suggesting it might be a potential anti-cancer drug in pancreatic cancer.

Differentiating lymphoma from lymphoid inflammatory hyperplasia using 18 F-FDG PET/CT radiomics combined with clinical features

Xie Liang1 , Qin Jialin1 , Wu Ruixue2 , Xiang Chunfeng3 , Fang Pengfei2 , Shou Chenfeng4 , Chen Hong5 , Pang Xiaoxi 1

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abstract:
To develop and to validate a combined model integrating 18 F-FDG PET/CT radiomics with clinical features to distinguish between lymphoma and lymphoid inflammatory hyperplasia. Methods A retrospec- tive study was conducted on a cohort of 232 patients diagnosed with lymphoma or lymphoid inflammatory hyperplasi- a. Comparative analyses of clinical and traditional imaging indicators were performed to identify inter-group differ- ences . The clinical features were delineated and extracted using medical software including 3DSlicer and Lifex . Se- lection of the features was performed to construct a PET/CT-based radiomics Logistic model , with a combined mod- el integrating PET/CT with clinical features then used to evaluate the discriminative efficacy of these models . Re- sults Analysis of inter-group differences indicated that age , CTmean , and metabolic tumor volume (MTV) were ef- fective for differentiating between lymphoma and lymphoid inflammatory hyperplasia ( P < 0. 05 ) . The PET/CT- based radiomics Logistic model differentiated between lymphoma and lymphoid inflammatory hyperplasia , with an area under curve (AUC) of 0. 924 (95% CI: 0. 884 - 0. 960) and 0. 863 (95% CI: 0. 774 - 0. 939) in the training and testing cohorts , respectively . The integrated Logistic model that combined PET/CT-based radiomics with clinical features to distinguish between lymphoma and lymphoid inflammatory hyperplasia achieved an AUC of 0. 933 (95% CI: 0. 889 - 0. 969) in the training cohort and 0. 884 (95% CI: 0. 792 - 0. 964) in the testing co- hort . Decision curve analysis (DCA) demonstrated that the integrated model provided the greatest clinical net ben- efit. Conclusion The hybrid model integrating 18 F-FDG PET/CT radiomics with clinical features shows robust di- agnostic efficacy to distinguish between lymphoma and lymphoid inflammatory hyperplasia.

Expression of HSPA8 in breast cancer and its biological function

Zhang Manman1 , Cheng Zheng1 , Zhou Jingni2 , Guo Qianying2 , Wu Zhengsheng1 , 2

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abstract:
To investigate the expression of HSPA8 in breast cancer and its effect on tumor biological behaviors . Methods Bioinformatics analysis and immunohistochemistry assays were used to detect the expression of HSPA8 in breast cancer and adjacent non-tumor breast tissues , and the relationship between its expression and clinicopathological characteristics of breast cancer patients was analyzed . Correlation between HSPA8 expression and prognosis of breast cancer patients was analyzed by Kaplan-Meier Plotter database . HSPA8 knockdown and overexpression breast cancer stabilized cells were constructed , respectively. CCK-8 , clone formation , Transwell , cell scratch , Western blot and immunofluorescence assay were used to detect the effects of HSPA8 on the prolifera- tion , invasion and migration of breast cancer cells , and its effect on epithelial-mesenchymal transition (EMT) . Results Bioinformatics analysis and immunohistochemistry assay revealed that the expression of HSPA8 in breast cancer tissues was higher than that in adjacent non-tumour tissues (P < 0. 05) , and its expression level of the pro- tein was significantly and positively correlated with the tumor size , histological grade , lymph node metastasis and Ki-67 proliferation index (P < 0. 05) . The Kaplan-Meier survival curve showed that high expression of HSPA8 was significantly associated with poor prognosis in breast cancer patients (P < 0. 05) . CCK-8 , clone formation , tran- swell , cell scratch , Western blot and immunofluorescence assay showed that knockdown of HSPA8 expression could significantly inhibit the proliferation , invasion , migration function and EMT of breast cancer cells ( P < 0. 05 ) , while overexpression of HSPA8 could significantly promote the proliferation , invasion , migration function and EMT of breast cancer cells ( P < 0. 05) . Conclusion HSPA8 is highly expressed in breast cancer tissues , which is closely related to disease progression and the malignant phenotype of breast cancer , suggesting that HSPA8 may be a potential biological target for breast cancer treatment.

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