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Article: Fungal communities associated with early immature tubers of wild

Li, Dong / Jin, Xiao-Han / Li, Yu / Wang, Yu-Chuan / He, Hai-Yan / Zhang, Han-Bo

2024 Volume 14, Issue 2, Page(s) e11004

Abstract: Full myco-heterotrophic ... ...

Abstract	Full myco-heterotrophic orchid
Language	English
Publishing date	2024-02-21
Publishing country	England
Document type	Journal Article
ZDB-ID	2635675-2
ISSN	2045-7758
ISSN	2045-7758
DOI	10.1002/ece3.11004
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Article ; Online: PHB promotes bladder cancer cell epithelial-mesenchymal transition via the Wnt/β-catenin signaling pathway.

Jiang, Li-Juan / Guo, Song-Bin / Huang, Zhong-Ying / Li, Xin-Ling / Jin, Xiao-Han / Huang, Wei-Juan / Tian, Xiao-Peng

Pathology, research and practice

2023 Volume 247, Page(s) 154536

Abstract: As a member of PHB (prohibitin1) family, PHB plays important roles in many cancers, but its property in bladder carcinoma aggressiveness is unknown. This research was to explore the function and potential mechanism of PHB in bladder carcinoma in vivo and ...

Abstract	As a member of PHB (prohibitin1) family, PHB plays important roles in many cancers, but its property in bladder carcinoma aggressiveness is unknown. This research was to explore the function and potential mechanism of PHB in bladder carcinoma in vivo and in vitro. The invasive abilities of cancer cell were determined by transwell and wound-healing assays. The function of PHB was confirmed by gene knockdown and overexpression methods. Further in vivo confirmation was performed in a nude mouse model with lung metastasis. The relationship of PHB and β-catenin was confirmed by immunoprecipitation and immunofluorescence staining assays. The protein expression of epithelial-mescenchymal transition (EMT) and Wnt/β-catenin signaling pathway was tested by immunofluorescence staining and western blotting assay. The depletion of PHB prevented bladder cancer cell invasiveness and inhibited EMT. Contrarily，the abilities of bladder carcinoma cells migration and invasion in vitro as well as metastasis in vivo were enhanced when the PHB overexpressed unnormally. Importantly, the β-catenin was identified to be bound by PHB and β-catenin knockdown reduced the cancer cell migration, invasion and EMT in PHB overexpressing cells. In addition, PHB stabilized β-catenin by inhibiting its ubiqutin-mediated degradation thus leading to increased Wnt/β-catenin signaling. These observations indicate that PHB could promote bladder cancer aggressiveness by binding with β-catenin to prevent the degradation of β-catenin and the localized invasive bladder cancer patients with PHB overexpression should take more aggressive postsurgical adjuvant anticancer therapies.
MeSH term(s)	Animals ; Mice ; beta Catenin/metabolism ; Wnt Signaling Pathway/genetics ; Urinary Bladder/pathology ; Epithelial-Mesenchymal Transition/genetics ; Neoplasm Invasiveness/pathology ; Urinary Bladder Neoplasms/genetics ; Carcinoma/genetics ; Cell Movement/genetics ; Cell Line, Tumor ; Cell Proliferation ; Gene Expression Regulation, Neoplastic
Chemical Substances	beta Catenin
Language	English
Publishing date	2023-05-16
Publishing country	Germany
Document type	Journal Article
ZDB-ID	391889-0
ISSN	1618-0631 ; 0344-0338
ISSN (online)	1618-0631
ISSN	0344-0338
DOI	10.1016/j.prp.2023.154536
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Article ; Online: Corrigendum to "AGBL2 promotes cancer cell growth through IRGM-regulated autophagy and enhanced Aurora A activity in hepatocellular carcinoma" [Canc. Lett. 414 (2018) 71-80].

Wang, Li-Li / Jin, Xiao-Han / Cai, Mu-Yan / Li, Hai-Gang / Chen, Jie-Wei / Wang, Feng-Wei / Wang, Chen-Yuan / Hu, Wei-Wei / Liu, Fang / Xie, Dan

Cancer letters

2022 Volume 539, Page(s) 215700

Language	English
Publishing date	2022-05-04
Publishing country	Ireland
Document type	Published Erratum
ZDB-ID	195674-7
ISSN	1872-7980 ; 0304-3835
ISSN (online)	1872-7980
ISSN	0304-3835
DOI	10.1016/j.canlet.2022.215700
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Zs.A 1177: Show issues

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Article ; Online: Genetic profile and biological implication of PIN2/TRF1-interacting telomerase inhibitor 1 (PinX1) in human cancers: an analysis using The Cancer Genome Atlas.

Huang, Wei-Juan / Li, Mei / Jin, Xiao-Han / Huang, Xiao-Jia / Zhao, Wei / Tian, Xiao-Peng

Oncotarget

2017 Volume 8, Issue 40, Page(s) 67241–67253

Abstract: Pin2/TRF1-interacting telomere inhibitor 1 (PinX1) was originally identified as a telomerase inhibitor, involved in maintaining telomerase activity, telomere length, and chromosomal stability. However, research has shown that PinX1 can have opposing ... ...

Abstract	Pin2/TRF1-interacting telomere inhibitor 1 (PinX1) was originally identified as a telomerase inhibitor, involved in maintaining telomerase activity, telomere length, and chromosomal stability. However, research has shown that PinX1 can have opposing molecular status in its expression patterns in several other tumor types. We thus investigated the genetic profile and biological implication of PinX1 in several human cancers using the cBioportal database. Our results showed that
Language	English
Publishing date	2017-09-15
Publishing country	United States
Document type	Journal Article
ZDB-ID	2560162-3
ISSN	1949-2553 ; 1949-2553
ISSN (online)	1949-2553
ISSN	1949-2553
DOI	10.18632/oncotarget.18589
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Article ; Online: Erratum: Acidic Microenvironment Up-Regulates Exosomal miR-21 and miR-10b in Early-Stage Hepatocellular Carcinoma to Promote Cancer Cell Proliferation and Metastasis: Erratum.

Tian, Xiao-Peng / Wang, Chen-Yuan / Jin, Xiao-Han / Li, Mei / Wang, Feng-Wei / Huang, Wei-Juan / Yun, Jing-Ping / Xu, Rui-Hua / Cai, Qing-Qing / Xie, Dan

Theranostics

2021 Volume 11, Issue 13, Page(s) 6522–6523

Abstract: This corrects the article DOI: 10.7150/thno.30958.]. ...

Abstract	[This corrects the article DOI: 10.7150/thno.30958.].
Language	English
Publishing date	2021-04-20
Publishing country	Australia
Document type	Published Erratum
ZDB-ID	2592097-2
ISSN	1838-7640 ; 1838-7640
ISSN (online)	1838-7640
ISSN	1838-7640
DOI	10.7150/thno.60140
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Article ; Online: The depletion of PinX1 involved in the tumorigenesis of non-small cell lung cancer promotes cell proliferation via p15/cyclin D1 pathway.

Tian, Xiao-Peng / Jin, Xiao-Han / Li, Mei / Huang, Wei-Juan / Xie, Dan / Zhang, Jia-Xing

Molecular cancer

2017 Volume 16, Issue 1, Page(s) 74

Abstract: Background: The telomerase/telomere interacting protein PinX1 has been suggested as a tumor suppressor. However, the clinical and biological significance of PinX1 in human non-small cell lung cancer (NSCLC) is unclear.: Methods: PinX1 gene/expression ...

Abstract	Background: The telomerase/telomere interacting protein PinX1 has been suggested as a tumor suppressor. However, the clinical and biological significance of PinX1 in human non-small cell lung cancer (NSCLC) is unclear. Methods: PinX1 gene/expression pattern and its association with NSCLC patient survival were analyzed in cBioportal Web resource and two cohorts of NSCLC samples. A series of in vivo and in vitro assays were performed to elucidate the function of PinX1 on NSCLC cells proliferation and underlying mechanisms. Results: More frequency of gene PinX1 homozygous deletion and heterozygote deficiency was first retrieved from cBioportal Web resource. Low expression of PinX1 correlated with smoking condition, histological type, T stage, N stage, M stage and TNM stage, and was an independent predictor for overall survival in a learning cohort (n = 93) and a validation cohort (n = 51) of NSCLC patients. Furthermore, knockdown of PinX1 dramatically accelerated NSCLC cell proliferation and G1/S transition, whereas ectopic overexpression of PinX1 substantially inhibited cell viability and cell cycle transition in vitro and in vivo. p15/cyclin D1 pathway and BMP5 might contribute to PinX1-associated cell proliferation and cell cycle transition. Conclusion: The cost-effective expression of PinX1 could constitute a novel molecular predictor/marker for NSCLC management.
MeSH term(s)	Adult ; Aged ; Animals ; Biomarkers, Tumor ; Bone Morphogenetic Protein 5/genetics ; Carcinoma, Non-Small-Cell Lung/genetics ; Carcinoma, Non-Small-Cell Lung/metabolism ; Carcinoma, Non-Small-Cell Lung/mortality ; Cell Cycle ; Cell Line, Tumor ; Cell Proliferation ; Cell Transformation, Neoplastic/genetics ; Cell Transformation, Neoplastic/metabolism ; Cyclin D1/metabolism ; Cyclin-Dependent Kinase Inhibitor p15/metabolism ; Databases, Nucleic Acid ; Disease Models, Animal ; Female ; Gene Deletion ; Gene Silencing ; Humans ; Lung Neoplasms/genetics ; Lung Neoplasms/metabolism ; Lung Neoplasms/mortality ; Male ; Mice ; Middle Aged ; Neoplasm Grading ; Neoplasm Staging ; Prognosis ; Signal Transduction ; Tumor Suppressor Proteins/genetics ; Xenograft Model Antitumor Assays
Chemical Substances	BMP5 protein, human ; Biomarkers, Tumor ; Bone Morphogenetic Protein 5 ; Cyclin-Dependent Kinase Inhibitor p15 ; PINX1 protein, human ; Tumor Suppressor Proteins ; Cyclin D1 (136601-57-5)
Language	English
Publishing date	2017-04-04
Publishing country	England
Document type	Journal Article
ISSN	1476-4598
ISSN (online)	1476-4598
DOI	10.1186/s12943-017-0637-4
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Article ; Online: ITLN1 inhibits tumor neovascularization and myeloid derived suppressor cells accumulation in colorectal carcinoma.

Chen, Li / Jin, Xiao-Han / Luo, Jie / Duan, Jin-Ling / Cai, Mu-Yan / Chen, Jie-Wei / Feng, Zi-Hao / Guo, Austin Meng / Wang, Feng-Wei / Xie, Dan

Oncogene

2021 Volume 40, Issue 40, Page(s) 5925–5937

Abstract: Low levels of ITLN1 have been correlated with obesity-related colorectal carcinogenesis, however, the specific functions and underlying mechanisms remain unclear. Thus, we sought to explore the inhibitory role of ITLN1 in the tumor-permissive ... ...

Abstract	Low levels of ITLN1 have been correlated with obesity-related colorectal carcinogenesis, however, the specific functions and underlying mechanisms remain unclear. Thus, we sought to explore the inhibitory role of ITLN1 in the tumor-permissive microenvironment that exists during the first occurrence and subsequent development of colorectal carcinoma (CRC). Results indicated that ITLN1 was frequently lost in CRC tissues and ITLN1 to be an independent prognostic predictor of CRC. Orthotopic and subcutaneous tumor xenograft approaches were then used to further confirm the protective role of ITLN1 during tumor progression. Increased ITLN1 expression in CRC cells significantly inhibited local pre-existing vessels sprouting, EPC recruitment and the infiltration of immunosuppressive myeloid-derived suppressor cells (MDSCs) into tumor tissues without affecting the behavior of CRC cells in vitro. Comparatively, ITLN1-derived MDSCs had a lower suppressive effect on T cell proliferation, NOS2 expression, and ROS production. In addition, ITLN1 overexpression markedly suppressed bone marrow (BM)-derived hematopoietic progenitor cells (HPC) differentiation into MDSCs as well as NOS2 activity on MDSCs. Using H-2b+YFP + chimerism through bone marrow transplantation, increased ITLN1 in HCT116 significantly reduced the BM-derived EPCs and MDSCs in vivo mobilization. Mechanistically, results indicated ITLN1 inhibited tumor-derived IL-17D and CXCL2 (MIP2) through the KEAP1/Nrf2/ROS/IL-17D and p65 NF-ĸB/CXCL2 signaling cascades dependent on PI3K/AKT/GSK3ß. This effect was reversed by the PI3K selective inhibitor LY294002. Collectively, ITLN1 synergistically suppressed IL-17D and CXCL2-mediated tumor vascularization, bone marrow derived EPC recruitment, as well as MDSCs generation and trafficking. Thus, ITLN1 potentially serves as a critical prognostic and therapeutic target for CRC.
MeSH term(s)	Animals ; Colorectal Neoplasms/genetics ; Colorectal Neoplasms/pathology ; Cytokines/metabolism ; GPI-Linked Proteins/metabolism ; Humans ; Lectins/metabolism ; Mice ; Myeloid-Derived Suppressor Cells/metabolism ; Neovascularization, Pathologic
Chemical Substances	Cytokines ; GPI-Linked Proteins ; Itln1 protein, mouse ; Lectins
Language	English
Publishing date	2021-08-06
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	639046-8
ISSN	1476-5594 ; 0950-9232
ISSN (online)	1476-5594
ISSN	0950-9232
DOI	10.1038/s41388-021-01965-5
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Zs.A 2218: Show issues

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Article ; Online: LZTFL1 inhibits kidney tumor cell growth by destabilizing AKT through ZNRF1-mediated ubiquitin proteosome pathway.

Oncogene

2023 Volume 42, Issue 19, Page(s) 1543–1557

Abstract: LZTFL1 is a tumor suppressor located in chromosomal region 3p21.3 that is deleted frequently and early in various cancer types including the kidney cancer. However, its role in kidney tumorigenesis remains unknown. Here we hypothesized a tumor ... ...

Abstract	LZTFL1 is a tumor suppressor located in chromosomal region 3p21.3 that is deleted frequently and early in various cancer types including the kidney cancer. However, its role in kidney tumorigenesis remains unknown. Here we hypothesized a tumor suppressive function of LZTFL1 in clear cell renal cell carcinoma (ccRCC) and its mechanism of action based on extensive bioinformatics analysis of patients' tumor data and validated it using both gain- and loss-functional studies in kidney tumor cell lines and patient-derive xenograft (PDX) model systems. Our studies indicated that LZTFL1 inhibits kidney tumor cell proliferation by destabilizing AKT through ZNRF1-mediated ubiquitin proteosome pathway and inducing cell cycle arrest at G1. Clinically, we found that LZTFL1 is frequently deleted in ccRCC. Downregulation of LZTFL1 is associated with a poor ccRCC outcome and may be used as prognostic maker. Furthermore, we show that overexpression of LZTFL1 in PDX via lentiviral delivery suppressed PDX growth, suggesting that re-expression of LZTFL1 may be a therapeutic strategy against ccRCC.
MeSH term(s)	Humans ; Carcinoma, Renal Cell/pathology ; Cell Line, Tumor ; Cell Proliferation ; Gene Expression Regulation, Neoplastic ; Kidney Neoplasms/pathology ; Proto-Oncogene Proteins c-akt/metabolism ; Transcription Factors/metabolism ; Ubiquitins/metabolism
Chemical Substances	LZTFL1 protein, human ; Proto-Oncogene Proteins c-akt (EC 2.7.11.1) ; Transcription Factors ; Ubiquitins ; ZNRF1 protein, human (EC 2.3.2.27)
Language	English
Publishing date	2023-03-25
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	639046-8
ISSN	1476-5594 ; 0950-9232
ISSN (online)	1476-5594
ISSN	0950-9232
DOI	10.1038/s41388-023-02666-x
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Article ; Online: KLF16 enhances stress tolerance of colorectal carcinomas by modulating nucleolar homeostasis and translational reprogramming.

Ma, Xiao-Dan / Xu, Shui-Dan / Hao, Shi-Hui / Han, Kai / Chen, Jie-Wei / Ling, Han / Chen, Ri-Xin / Jin, Xiao-Han / Cao, Jing-Hua / Lin, Jin-Long / Ou, Qing-Jian / Fang, Yu-Jing / Pan, Zhi-Zhong / Xie, Dan / Wang, Feng-Wei

Molecular therapy : the journal of the American Society of Gene Therapy

2022 Volume 30, Issue 8, Page(s) 2828–2843

Abstract: Translational reprogramming is part of the unfolded protein response (UPR) during endoplasmic reticulum (ER) stress, which acts to the advantage of cancer growth and development in different stress conditions, but the mechanism of ER stress-related ... ...

Abstract	Translational reprogramming is part of the unfolded protein response (UPR) during endoplasmic reticulum (ER) stress, which acts to the advantage of cancer growth and development in different stress conditions, but the mechanism of ER stress-related translational reprogramming in colorectal carcinoma (CRC) progression remains unclear. Here, we identified that Krüppel-like factor 16 (KLF16) can promote CRC progression and stress tolerance through translational reprogramming. The expression of KLF16 was upregulated in CRC tissues and associated with poor prognosis for CRC patients. We found that ER stress inducers can recruit KLF16 to the nucleolus and increase its interaction with two essential proteins for nucleolar homeostasis: nucleophosmin1 (NPM1) and fibrillarin (FBL). Moreover, knockdown of KLF16 can dysregulate nucleolar homeostasis in CRC cells. Translation-reporter system and polysome profiling assays further showed that KLF16 can effectively promote cap-independent translation of ATF4, which can enhance ER-phagy and the proliferation of CRC cells. Overall, our study unveils a previously unrecognized role for KLF16 as an ER stress regulator through mediating translational reprogramming to enhance the stress tolerance of CRC cells and provides a potential therapeutic vulnerability.
MeSH term(s)	Colorectal Neoplasms/genetics ; Colorectal Neoplasms/metabolism ; Endoplasmic Reticulum Stress/genetics ; Homeostasis ; Humans ; Kruppel-Like Transcription Factors/genetics ; Kruppel-Like Transcription Factors/metabolism ; Unfolded Protein Response
Chemical Substances	KLF16 protein, human ; Kruppel-Like Transcription Factors
Language	English
Publishing date	2022-05-05
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2010592-7
ISSN	1525-0024 ; 1525-0016
ISSN (online)	1525-0024
ISSN	1525-0016
DOI	10.1016/j.ymthe.2022.04.022
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Article ; Online: ACT001 can prevent and reverse tamoxifen resistance in human breast cancer cell lines by inhibiting NF-κB activation.

Jin, Xiao-Han / Jia, Yong-Sheng / Shi, Ye-Hui / Li, Qiu-Ying / Bao, Shi-Qi / Lu, Wen-Ping / Tong, Zhong-Sheng

Journal of cellular biochemistry

2018 Volume 120, Issue 2, Page(s) 1386–1397

Abstract: Endocrine therapy is one of the main treatments for estrogen receptor-positive breast cancers. Tamoxifen is the most commonly used drug for endocrine therapy. However, primary or acquired tamoxifen resistance occurs in a large proportion of breast cancer ...

Abstract	Endocrine therapy is one of the main treatments for estrogen receptor-positive breast cancers. Tamoxifen is the most commonly used drug for endocrine therapy. However, primary or acquired tamoxifen resistance occurs in a large proportion of breast cancer patients, leading to therapeutic failure. We found that the combination of tamoxifen and ACT001, a nuclear factor-κB (NF-κB) signaling pathway inhibitor, effectively inhibited the proliferation of both tamoxifen-sensitive and tamoxifen-resistant cells. The tamoxifen-resistant cell line MCF7R/LCC9 showed active NF-κB signaling and high apoptosis-related gene transcription, especially for antiapoptotic genes, which could be diminished by treatment with ACT001. These results demonstrate that ACT001 can prevent and reverse tamoxifen resistance by inhibiting NF-κB activation.
Language	English
Publishing date	2018-11-18
Publishing country	United States
Document type	Journal Article
ZDB-ID	392402-6
ISSN	1097-4644 ; 0730-2312
ISSN (online)	1097-4644
ISSN	0730-2312
DOI	10.1002/jcb.27146
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