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Article ; Online: Early diagnosis of cancer using circulating microbial DNA.

Law, Helen Ka Wai / Yim, Howard Chi Ho

Cell reports. Medicine

2024 Volume 5, Issue 4, Page(s) 101502

Abstract: The study by Chen et al. has advanced research by developing predictive models based on circulating microbial DNA, offering potential for early cancer detection and personalized treatment. However, further validation and simplification of techniques are ... ...

Abstract	The study by Chen et al. has advanced research by developing predictive models based on circulating microbial DNA, offering potential for early cancer detection and personalized treatment. However, further validation and simplification of techniques are needed for widespread clinical application.
MeSH term(s)	Humans ; Cell-Free Nucleic Acids ; Early Detection of Cancer/methods ; Neoplasms/genetics ; DNA
Chemical Substances	Cell-Free Nucleic Acids ; DNA (9007-49-2)
Language	English
Publishing date	2024-04-16
Publishing country	United States
Document type	Journal Article
ISSN	2666-3791
ISSN (online)	2666-3791
DOI	10.1016/j.xcrm.2024.101502
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Article: Deciphering the role of autophagy in the immunopathogenesis of inflammatory bowel disease.

Li, Yue / Law, Helen Ka Wai

Frontiers in pharmacology

2022 Volume 13, Page(s) 1070184

Abstract: Inflammatory bowel disease (IBD) is a typical immune-mediated chronic inflammatory disorder. Following the industrialization and changes in lifestyle, the incidence of IBD in the world is rising, which makes health concerns and heavy burdens all over the ...

Abstract	Inflammatory bowel disease (IBD) is a typical immune-mediated chronic inflammatory disorder. Following the industrialization and changes in lifestyle, the incidence of IBD in the world is rising, which makes health concerns and heavy burdens all over the world. However, the pathogenesis of IBD remains unclear, and the current understanding of the pathogenesis involves dysregulation of mucosal immunity, gut microbiome dysbiosis, and gut barrier defect based on genetic susceptibility and environmental triggers. In recent years, autophagy has emerged as a key mechanism in IBD development and progression because Genome-Wide Association Study revealed the complex interactions of autophagy in IBD, especially immunopathogenesis. Besides, autophagy markers are also suggested to be potential biomarkers and target treatment in IBD. This review summarizes the autophagy-related genes regulating immune response in IBD. Furthermore, we explore the evolving evidence that autophagy interacts with intestinal epithelial and immune cells to contribute to the inflammatory changes in IBD. Finally, we discuss how novel discovery could further advance our understanding of the role of autophagy and inform novel therapeutic strategies in IBD.
Language	English
Publishing date	2022-11-14
Publishing country	Switzerland
Document type	Journal Article ; Review
ZDB-ID	2587355-6
ISSN	1663-9812
ISSN	1663-9812
DOI	10.3389/fphar.2022.1070184
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Article: Psychosocial needs of post-radiotherapy cancer survivors and their direct caregivers - a systematic review.

Man, Ka Hei / Law, Helen Ka-Wai / Tam, Shing Yau

Frontiers in oncology

2023 Volume 13, Page(s) 1246844

Abstract: Radiotherapy is an important modality for cancer treatment. About 50% of cancer patients receive radiotherapy, and one-third of radiotherapy recipients were identified as having unmet psychosocial needs. The unmet psychosocial needs worsen the patient's ... ...

Abstract	Radiotherapy is an important modality for cancer treatment. About 50% of cancer patients receive radiotherapy, and one-third of radiotherapy recipients were identified as having unmet psychosocial needs. The unmet psychosocial needs worsen the patient's quality of life and treatment effectiveness. This review aims to identify the psychosocial needs of post-radiotherapy cancer survivors and their direct caregivers. Systematic research of Embase, Scopus and PubMed was done and 17 studies were selected for analysis. The results show that patients encounter distress and fear due to treatment immobilization and unfamiliarity with procedures respectively. Information provision is a common need raised by patients and caregivers. Patients and caregivers report relationship problems due to affected sexual functions. To facilitate future studies, solutions to each identified psychosocial need are proposed in the discussion based on the 17 selected papers and other supporting literature. This review proposes art therapy to alleviate psychological distress, and pre-treatment information sessions to reinforce information delivery. Creative interventions such as a sexual rehabilitation program are recommended. Future studies are warranted to examine the interventions and thus improve the patients' and caregivers' well-being.
Language	English
Publishing date	2023-10-26
Publishing country	Switzerland
Document type	Systematic Review
ZDB-ID	2649216-7
ISSN	2234-943X
ISSN	2234-943X
DOI	10.3389/fonc.2023.1246844
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Article ; Online: Suppression of small nucleolar RNA host gene 8 (SNHG8) inhibits the progression of colorectal cancer cells.

Islam Khan, Md Zahirul / Law, Helen Ka Wai

Non-coding RNA research

2023 Volume 8, Issue 2, Page(s) 224–232

Abstract: Colorectal cancer (CRC) is one of the most common gastrointestinal malignancies around the world with high mortality. Accumulating evidences demonstrate that long non-coding RNAs (lncRNAs) play critical roles in CRC tumorigenesis by regulating different ... ...

Abstract	Colorectal cancer (CRC) is one of the most common gastrointestinal malignancies around the world with high mortality. Accumulating evidences demonstrate that long non-coding RNAs (lncRNAs) play critical roles in CRC tumorigenesis by regulating different pathways of carcinogenesis. SNHG8 (small nucleolar RNA host gene 8), a lncRNA, is highly expressed in several cancers and acts as an oncogene that promotes cancer progression. However, the oncogenic role of SNHG8 in CRC carcinogenesis and the underlying molecular mechanisms remain unknown. In this study, we explored the role of SNHG8 in CRC cell lines by performing a series of functional experiments. Similar to the data reported in the Encyclopedia of RNA Interactome, our RT-qPCR results showed that SNHG8 expression was significantly upregulated in CRC cell lines (DLD-1, HT-29, HCT-116, and SW480) compared to the normal colon cell line (CCD-112CoN). We performed dicer-substrate siRNA transfection to knockdown the expression of SNHG8 in HCT-116 and SW480 cell lines which were expressing high levels of SNHG8. SNHG8 knockdown significantly reduced CRC cell growth and proliferation by inducing autophagy and apoptosis pathways through the AKT/AMPK/mTOR axis. We performed wound healing migration assay and demonstrated that SNHG8 knockdown significantly increased migration index in both cell lines, indicating reduced migration abilities of cells. Further investigation showed that SNHG8 knockdown suppresses epithelial to mesenchymal transition and reduces cellular migratory properties of CRC cells. Taken together, our study suggests that SNHG8 acts as an oncogene in CRC through the mTOR-dependent autophagy, apoptosis, and EMT pathways. Our study provides a better understanding the role of SNHG8 in CRC at molecular level and SNHG8 might be used as novel therapeutic target for CRC management.
Language	English
Publishing date	2023-02-14
Publishing country	Netherlands
Document type	Journal Article
ISSN	2468-0540
ISSN (online)	2468-0540
DOI	10.1016/j.ncrna.2023.02.003
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Article ; Online: Advances in High Throughput Proteomics Profiling in Establishing Potential Biomarkers for Gastrointestinal Cancer.

Islam Khan, Md Zahirul / Tam, Shing Yau / Law, Helen Ka Wai

Cells

2022 Volume 11, Issue 6

Abstract: Gastrointestinal cancers (GICs) remain the most diagnosed cancers and accounted for the highest cancer-related death globally. The prognosis and treatment outcomes of many GICs are poor because most of the cases are diagnosed in advanced metastatic ... ...

Abstract	Gastrointestinal cancers (GICs) remain the most diagnosed cancers and accounted for the highest cancer-related death globally. The prognosis and treatment outcomes of many GICs are poor because most of the cases are diagnosed in advanced metastatic stages. This is primarily attributed to the deficiency of effective and reliable early diagnostic biomarkers. The existing biomarkers for GICs diagnosis exhibited inadequate specificity and sensitivity. To improve the early diagnosis of GICs, biomarkers with higher specificity and sensitivity are warranted. Proteomics study and its functional analysis focus on elucidating physiological and biological functions of unknown or annotated proteins and deciphering cellular mechanisms at molecular levels. In addition, quantitative analysis of translational proteomics is a promising approach in enhancing the early identification and proper management of GICs. In this review, we focus on the advances in mass spectrometry along with the quantitative and functional analysis of proteomics data that contributes to the establishment of biomarkers for GICs including, colorectal, gastric, hepatocellular, pancreatic, and esophageal cancer. We also discuss the future challenges in the validation of proteomics-based biomarkers for their translation into clinics.
MeSH term(s)	Biomarkers ; Gastrointestinal Neoplasms/diagnosis ; Gastrointestinal Neoplasms/metabolism ; Humans ; Mass Spectrometry/methods ; Proteomics/methods
Chemical Substances	Biomarkers
Language	English
Publishing date	2022-03-11
Publishing country	Switzerland
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	2661518-6
ISSN	2073-4409 ; 2073-4409
ISSN (online)	2073-4409
ISSN	2073-4409
DOI	10.3390/cells11060973
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Article ; Online: Immune Complexes Impaired Glomerular Endothelial Cell Functions in Lupus Nephritis.

Wang, Linlin / Law, Helen Ka Wai

International journal of molecular sciences

2019 Volume 20, Issue 21

Abstract: Lupus nephritis (LN) is one of the most common and severe complications of lupus. However, the mechanisms for renal damage have not been well elucidated. There are evidences show that glomerular endothelial cells (GECs) are damaged in LN. Immune ... ...

Abstract	Lupus nephritis (LN) is one of the most common and severe complications of lupus. However, the mechanisms for renal damage have not been well elucidated. There are evidences show that glomerular endothelial cells (GECs) are damaged in LN. Immune complexes can deposit in subendothelial area and could affect GEC functions. In the present study, we used heat-aggregated gamma globulin (HAGG) to simulate immune complexes and investigated their effects on GEC functions. Our results revealed that HAGG impaired different aspect of the GEC functions. HAGG changed cell morphology, upregulated the expression of active caspase-3, inhibited angiogenesis, and increased NO production in GECs. These results provide new clues for the mechanisms of renal damage and the pathology of LN.
MeSH term(s)	Caspase 3/metabolism ; Cells, Cultured ; Endothelial Cells/cytology ; Endothelial Cells/drug effects ; Endothelial Cells/metabolism ; Hot Temperature ; Humans ; Kidney Glomerulus/cytology ; Lupus Nephritis/metabolism ; Lupus Nephritis/pathology ; Necrosis ; Neovascularization, Physiologic/drug effects ; Nitric Oxide/metabolism ; Tumor Necrosis Factor-alpha/pharmacology ; Up-Regulation/drug effects ; gamma-Globulins/immunology ; gamma-Globulins/pharmacology
Chemical Substances	Tumor Necrosis Factor-alpha ; gamma-Globulins ; Nitric Oxide (31C4KY9ESH) ; Caspase 3 (EC 3.4.22.-)
Language	English
Publishing date	2019-10-24
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2019364-6
ISSN	1422-0067 ; 1422-0067 ; 1661-6596
ISSN (online)	1422-0067
ISSN	1422-0067 ; 1661-6596
DOI	10.3390/ijms20215281
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Article: JNK in Tumor Microenvironment: Present Findings and Challenges in Clinical Translation.

Tam, Shing Yau / Law, Helen Ka-Wai

Cancers

2021 Volume 13, Issue 9

Abstract: The c-Jun N-terminal kinases (JNKs) are a group of mitogen-activated protein kinases (MAPKs). JNK is mainly activated under stressful conditions or by inflammatory cytokines and has multiple downstream targets for mediating cell proliferation, ... ...

Abstract	The c-Jun N-terminal kinases (JNKs) are a group of mitogen-activated protein kinases (MAPKs). JNK is mainly activated under stressful conditions or by inflammatory cytokines and has multiple downstream targets for mediating cell proliferation, differentiation, survival, apoptosis, and immune responses. JNK has been demonstrated to have both tumor promoting and tumor suppressing roles in different cancers depending on the focused pathway in each study. JNK also plays complex roles in the heterogeneous tumor microenvironment (TME). JNK is involved in different tumorigenesis pathways. TME closely relates with tumor development and consists of various stressful and chronic inflammatory conditions along with different cell populations, in which the JNK pathway may have various mediating roles. In this review, we aim to summarize the present knowledge of JNK-mediated processes in TME, including hypoxia, reactive oxygen species, inflammation, immune responses, angiogenesis, as well as the regulation of various cell populations within TME. This review also suggests future research directions for translating JNK modulation in pre-clinical findings to clinical benefits.
Language	English
Publishing date	2021-05-03
Publishing country	Switzerland
Document type	Journal Article ; Review
ZDB-ID	2527080-1
ISSN	2072-6694
ISSN	2072-6694
DOI	10.3390/cancers13092196
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Article: Cancer Susceptibility Candidate 9 (CASC9) Promotes Colorectal Cancer Carcinogenesis via mTOR-Dependent Autophagy and Epithelial-Mesenchymal Transition Pathways.

Islam Khan, Md Zahirul / Law, Helen Ka Wai

Frontiers in molecular biosciences

2021 Volume 8, Page(s) 627022

Abstract: Background: Colorectal cancer (CRC) is the third most common cancer worldwide. Many recent studies have demonstrated that different long non-coding RNAs (lncRNAs) are involved in the initiation, advancement, and metastasis of many cancers including CRC. ...

Abstract	Background: Colorectal cancer (CRC) is the third most common cancer worldwide. Many recent studies have demonstrated that different long non-coding RNAs (lncRNAs) are involved in the initiation, advancement, and metastasis of many cancers including CRC. Cancer susceptibility candidate 9 (CASC9) is an lncRNA that has been reported in many cancers, but its role in CRC is poorly understood. In this study, we aimed to examine the expression of CASC9 in CRC cell lines and to determine the mechanism of action of CASC9 in CRC carcinogenesis. Methods: The expression of CASC9 in CRC tissues was compared with normal samples from publicly available datasets in The Cancer Genome Atlas (TCGA) and The Encyclopedia of RNA Interactomes (ENCORI). CASC9 expression was further verified in four CRC cell lines (DLD1, HT-29, SW480, and HCT-116) and normal colorectal cell line (CCD-112CoN) by real-time quantitative polymerase chain reaction (RT-qPCR). After gene silencing in HCT-116 and SW480, Cell Counting Kit-8 assay, clonogenic assay, and wound healing assay were performed to evaluate cell proliferation, viability, and migration index of cells. Western blotting was used to explore the key pathways involved. Results: CASC9 was significantly upregulated as analyzed from both public datasets TCGA and ENCORI where its overexpression was associated with poor survival of CRC patients. Similarly, CASC9 was significantly overexpressed in the CRC cell lines compared with normal cells studied. The silencing of CASC9 in HCT-116 and SW480 attenuated cell proliferation and migration significantly. Furthermore, pathways investigations showed that silencing of CASC9 significantly induced autophagy, promoted AMP-activated protein kinase (AMPK) phosphorylation, inhibited mTOR and AKT signaling pathways, and altered epithelial-mesenchymal transition (EMT) marker protein expression. Conclusion: We demonstrated that silencing of CASC9 contributes to the reduced CRC cell proliferation and migration by regulating autophagy and AKT/mTOR/EMT signaling. Therefore, CASC9 plays an important role in carcinogenesis, and its expression may act as a prognostic biomarker and a potential therapeutic target of CRC management.
Language	English
Publishing date	2021-05-04
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2814330-9
ISSN	2296-889X
ISSN	2296-889X
DOI	10.3389/fmolb.2021.627022
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Article: RAMS11 promotes CRC through mTOR-dependent inhibition of autophagy, suppression of apoptosis, and promotion of epithelial-mesenchymal transition.

Islam Khan, Md Zahirul / Law, Helen Ka Wai

Cancer cell international

2021 Volume 21, Issue 1, Page(s) 321

Abstract: Background: Long non-coding RNAs (lncRNAs), a class of non-coding RNAs (ncRNAs) associated with diverse biological processes of cells. Over the past decades, cumulating research evidences revealed that abnormal expressions of lncRNAs are associated with ...

Abstract	Background: Long non-coding RNAs (lncRNAs), a class of non-coding RNAs (ncRNAs) associated with diverse biological processes of cells. Over the past decades, cumulating research evidences revealed that abnormal expressions of lncRNAs are associated with colorectal cancer (CRC) initiation, progression, metastasis, and resistance to therapies. Moreover, their usefulness as candidate biomarkers for CRC diagnosis and prognosis are well evident throughout previous literature. In the current study, we examined the role and molecular mechanisms of newly identified lncRNA named RNA associated with metastasis-11 (RAMS11) in CRC development. Methods: The expression of RAMS11 in CRC cell lines DLD-1, HT-29, HCT-116, and SW480 and colon normal cells CCD-112-CoN were evaluated by quantitative RT-qPCR. The results showed that the RAMS11 is significantly upregulated in CRC cell lines compared to the normal cells. The CCK-8 proliferation assay, colony formation assay, and migration assay were performed to evaluate the biological and physiological functions of RAMS11 in vitro. To decipher the molecular mechanisms of RAMS11 medicated CRC progression, we further performed western blot analysis of the key pathway proteins (e.g., AMPK, AKT, and mTOR). Results: Our results revealed that higher expression of RAMS11 is associated with increased CRC proliferation, migration, and development of metastasis. Knockdown of RAMS11 induced autophagy, apoptosis along with reduction of epithelial-mesenchymal transition (EMT) suggesting that RAMS11 is involved in CRC progression. The molecular mechanisms of RAMS11 indicated that knockdown of RAMS11 significantly inhibited CRC carcinogenesis through mTOR-dependent autophagy induction. Conclusions: In sum, our results suggested that RAMS11 is an important oncogene in CRC pathogenesis. Targeting RAMS11 could be a potential therapeutic strategy for CRC management.
Language	English
Publishing date	2021-06-26
Publishing country	England
Document type	Journal Article
ZDB-ID	2091573-1
ISSN	1475-2867
ISSN	1475-2867
DOI	10.1186/s12935-021-02023-6
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Article ; Online: Immune complexes suppressed autophagy in glomerular endothelial cells.

Wang, Linlin / Law, Helen Ka Wai

Cellular immunology

2018 Volume 328, Page(s) 1–8

Abstract: Lupus nephritis is an immune-complexes mediated glomerulonephritis. Vascular lesions and endothelial cell injuries are common in lupus nephritis and important for renal damage. However, the precise mechanisms by which immune complexes lead to endothelial ...

Abstract	Lupus nephritis is an immune-complexes mediated glomerulonephritis. Vascular lesions and endothelial cell injuries are common in lupus nephritis and important for renal damage. However, the precise mechanisms by which immune complexes lead to endothelial cell injuries are still unclear. Autophagy is a conserved metabolic process and shows protective roles in many cell types and diseases. In present study, we investigated whether immune complexes could affect autophagy and participate in endothelial dysfunctions. Heat-aggregated gamma globulin (HAGG) was used to substitute immune complexes. Glomerular endothelial cells (GECs) were incubated with HAGG and autophagy-related markers were evaluated. Results showed that HAGG suppressed autophagy in GECs, through Akt/mTOR-dependent pathway. The combination of HAGG and tumor necrosis factor-alpha suppressed autophagy in GECs and further decreased cell viabilities. The suppressed effects of HAGG on GECs autophagy and viability, especially under inflammatory microenvironment, may provide new views for explaining the mechanisms of renal impairments in lupus nephritis.
MeSH term(s)	Antigen-Antibody Complex/immunology ; Autophagy/immunology ; Cell Survival/immunology ; Endothelial Cells/immunology ; Endothelial Cells/physiology ; Glomerulonephritis/physiopathology ; Humans ; Immunoglobulins, Intravenous ; Kidney/immunology ; Kidney/physiology ; Lupus Nephritis/immunology ; Lupus Nephritis/physiopathology ; Primary Cell Culture ; Proto-Oncogene Proteins c-akt/metabolism ; TOR Serine-Threonine Kinases/metabolism ; Tumor Necrosis Factor-alpha/metabolism ; gamma-Globulins/metabolism
Chemical Substances	Antigen-Antibody Complex ; Immunoglobulins, Intravenous ; Tumor Necrosis Factor-alpha ; gamma-Globulins ; TOR Serine-Threonine Kinases (EC 2.7.1.1) ; Proto-Oncogene Proteins c-akt (EC 2.7.11.1)
Language	English
Publishing date	2018-02-21
Publishing country	Netherlands
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	80094-6
ISSN	1090-2163 ; 0008-8749
ISSN (online)	1090-2163
ISSN	0008-8749
DOI	10.1016/j.cellimm.2018.02.013
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