Xiaoxiao Liu — Researcher Analysis Report
Analysis Mode: fast | Analysis Time: 2026-03-16T00:47:49
Rating: Active Researcher (40.2/100)
Basic Metrics
| Metric | Value |
|---|---|
| Institution | Unknown |
| h-index | 12 |
| Total Citations | 451 |
| Recent 5 Years Citations | 174 |
| Total Papers | 23 |
| Papers in Top Conferences | 0 |
| Publication Period | 2005 - 2023 |
| Semantic Scholar | 46522031 |
Research Trajectory
It should be noted first: there is a clear name disambiguation issue in this paper list. The papers span completely unrelated fields such as cancer biology, GPU architecture, plant immunity, hyperspectral image processing, genomics, and LLM prompt engineering. Clearly, they originate from the aggregation of multiple researchers with the same name. Based on publication years, citation counts, and thematic coherence, at least 3 different Xiaoxiao Liu can be identified: (1) in the field of molecular oncology (contributing most of the 451 citations, including the highest-cited paper on miR-1271 pancreatic cancer with 62 citations and papers at the level of Nature Communications/JEM/PNAS); (2) in computer architecture/image processing (GPU memory design, hyperspectral denoising); (3) in LLM/AI safety (prompt engineering and safety evaluation from 2023–2025). The following analysis mainly focuses on the most representative and best-documented molecular oncology researcher, whose research trajectory shows a gradual progression from microRNA regulation → p53-MDM2 targeted therapy → E3 ubiquitin ligase tumor suppression → CHIP clonal hematopoiesis.
Breakthrough Work
1. miR-1271 inhibits migration, invasion, and epithelial-mesenchymal transition by targeting ZEB1 and TWIST1 in pancreatic cancer cells (2016)
Description: For the first time, it systematically elucidated that miR-1271 suppresses the migration, invasion, and epithelial-mesenchymal transition of pancreatic cancer cells by simultaneously targeting two core EMT transcription factors, ZEB1 and TWIST1, providing a dual-target miRNA regulatory framework for the metastasis mechanism of pancreatic cancer.
Why it couldn’t be done before: Before 2016, the cost of high-throughput sequencing of miRNAs was too high, and systematic studies on the miRNA regulatory networks in pancreatic cancer were limited; the mechanism by which ZEB1 and TWIST1 were co-targeted by the same miRNA had not been revealed. Only with the popularization of NGS technology and the maturity of bioinformatics analysis tools was it possible to systematically screen and verify this dual-target regulatory axis.
Impact: The paper with 62 citations, which is the highest-cited paper by this researcher, promoted the establishment of multi-target miRNA regulatory strategies in pancreatic cancer metastasis research and has important reference value for subsequent studies on EMT-related therapeutic targets.
2. Antitumor immunity enhances the therapeutic effects of p53 activation on acute myeloid leukemia (2019)
Description: Published in Nature Communications, it demonstrated that the oral active p53-MDM2 interaction inhibitor DS-5272 not only exerts antitumor effects by directly activating the p53 signal in AML cells but also synergizes with the host’s antitumor immune response, revealing the synergistic mechanism between targeted therapy and tumor immunity.
Why it couldn’t be done before: p53-MDM2 inhibitors were long considered to act through cellular autonomous pathways, and the long-standing separation between oncology and targeted drug research made it difficult to discover this synergy. Around 2019, the integration of immun oncology and small molecule targeted therapy became a research hotspot. The maturity of single-cell typing technologies such as CyTOF (with supporting datasets published in the same year) made it possible to accurately quantify the dynamic changes in immune cell subsets.
Impact: Published in Nature Communications with 42 citations, it expanded p53-targeted therapy research in AML from a single cell killing paradigm to the immune regulatory dimension, providing a theoretical basis for the design of clinical combination immune checkpoint inhibitor regimens later on.
3. Mutational inactivation of mTORC1 repressor gene DEPDC5 in human gastrointestinal stromal tumors (2019)
Description: Published in PNAS, it reported for the first time that mutation-induced inactivation of the mTORC1 negative regulatory gene DEPDC5 is an important driver of GIST progression (rather than initiation), and clarified a new molecular mechanism for the malignant progression of GIST after KIT/PDGFRA mutations.
Why it couldn’t be done before: DEPDC5 had been mainly studied in neurological diseases (such as focal epilepsy), and its association with GIST had not been discovered for a long time. Research on the progression mechanism of GIST requires large-scale genomic sequencing data; the large-scale application of next-generation sequencing in clinical tumor samples, combined with a systematic research design on the evolutionary trajectory of ‘micro-GIST→progressing GIST’, is a prerequisite for this discovery.
Impact: Published with 34 citations, it provided a new explanation for the progression mechanism after GIST targeted therapy resistance, and the mTOR pathway entered the candidate list of GIST treatment targets, having direct clinical translation value.
4. E3 ligase MKRN3 is a tumor suppressor regulating PABPC1 ubiquitination in non–small cell lung cancer (2021)
Description: Published in Journal of Experimental Medicine, it found that the pathogenic gene MKRN3 for central precocious puberty is a true tumor suppressor in NSCLC, and it regulates global protein synthesis through targeting PABPC1 ubiquitination modification, revealing a completely new ‘E3 ligase-mRNA-binding protein-proteome homeostasis’ tumor suppression axis.
Why it couldn’t be done before: MKRN3 was previously recognized only as a developmental regulation gene, and its function in tumors was completely unknown. This discovery required a unique perspective of cross-referencing clinical genetics of central precocious puberty with cancer genomics databases, as well as mature ubiquitomics protein profiling techniques to identify PABPC1 as a substrate. This cognitive leap from ‘endocrine disease gene→tumor suppressor’ depends on the completeness of large-scale cancer genome maps (such as TCGA) databases.
Impact: Published with 41 citations, it provided a new tumor suppression mechanism and potential therapeutic targets for NSCLC, while also creating a new paradigm for studying ‘reuse of developmental genes in tumors’.
5. CHIP-associated mutant ASXL1 in blood cells promotes solid tumor progression (2022)
Description: It revealed that CHIP-related mutant ASXL1 in blood cells promotes solid tumor progression, establishing a causal relationship between clonal hematopoiesis (CHIP) clone mutations and non-hematopoietic system tumors, providing important evidence for CHIP-cross-system tumor effects research.
Why it couldn’t be done before: The recognition of CHIP as an independent risk factor itself was established only in 2014–2017 with large-scale population cohort studies. Associating CHIP with solid tumor progression requires simultaneously having accurate CHIP mouse models, a solid tumor transplantation system, and a deep understanding of the functions of bone marrow-derived cells in the tumor microenvironment. These technical and cognitive conditions matured synchronously around 2022.
Impact: Published with 30 citations, it expanded CHIP research from cardiovascular diseases and blood malignancy risks to solid tumors, having important clinical significance for risk stratification and treatment strategy formulation in elderly cancer patients.
Research Directions
- Synergistic mechanism between AML/MDS targeted therapy and tumor immunity (p53-MDM2, IMPDH inhibition)
- Functional studies of E3 ubiquitin ligases in tumors (STUB1/RUNX1, MKRN3/PABPC1)
- Molecular driving mechanisms and new target discovery for solid tumors (GIST, NSCLC, pancreatic cancer)
- Role of microRNAs in cancer metastasis and EMT regulation
- Cross-system effects of clonal hematopoiesis (CHIP) and tumor progression
Methodological Evolution
Early (2005–2016) focused mainly on single molecular mechanism studies, using classic cell line experiments + overexpression/knockdown validation paradigms to study miRNA target gene regulation. From 2017–2019, a integrated research strategy was adopted, introducing mouse in vivo models, drug intervention experiments, and cell typing (CyTOF), achieving a transition from ‘mechanism discovery’ to ‘therapeutic validation’. A representative example is the AML research published in Nature Communications. From 2020–2022, it was further upgraded to a dual-layer strategy of systematic screening + mechanism deep analysis: using CRISPR functional genomics screening or ubiquitomics mass spectrometry to discover targets (such as CDK1 screening, MKRN3-PABPC1 axis), followed by validation with patient sample databases to check clinical relevance. The methodological maturity significantly improved.
Field Impact
The core contributions of this researcher in molecular oncology focus on three aspects: (1) promoted the paradigm shift of AML targeted therapy from pure cell killing to a ‘targeted + immune synergy’ model; (2) systematically expanded the understanding of E3 ubiquitin ligases as tumor suppressors in solid tumors, especially the discovery of MKRN3 effectively connecting developmental biology and oncology; (3) provided new molecular targets and treatment strategies for refractory tumors such as GIST and NSCLC. Overall, this researcher is a stable contributor in the intersection of hematological tumors and solid tumors, with publications in high-impact journals such as JEM, Nature Communications, PNAS, EMBO Molecular Medicine. However, it should be noted that its h-index 12 is relatively low compared to the number of papers and top journals. Part of the reason may be data distortion due to name aggregation, and the actual academic influence of a single researcher may be underestimated.
Highly Cited Papers (Top 20)| # | Year | Reference | Title |
|—|——|——|——| | 1 | 2016 | 62 | miR-1271 inhibits migration, invasion and epithelial-mesenchymal transition by targeting ZEB1 and TWIST1 in pancreatic cancer cells. | | 2 | 2019 | 42 | Antitumor immunity augments the therapeutic effects of p53 activation on acute myeloid leukemia | | 3 | 2021 | 41 | E3 ligase MKRN3 is a tumor suppressor regulating PABPC1 ubiquitination in non–small cell lung cancer | | 4 | 2019 | 34 | Mutational inactivation of mTORC1 repressor gene DEPDC5 in human gastrointestinal stromal tumors | | 5 | 2021 | 33 | Integrated Screens Identify CDK1 as a Therapeutic Target in Advanced Gastrointestinal Stromal Tumors | | 6 | 2022 | 30 | CHIP‑associated mutant ASXL1 in blood cells promotes solid tumor progression | | 7 | 2018 | 29 | miRNA-199a-5p suppresses proliferation and invasion by directly targeting NF-κB1 in human ovarian cancer cells. | | 8 | 2021 | 29 | Advances in Targeted Therapy and Immunotherapy for Pancreatic Cancer. | | 9 | 2022 | 29 | IMPDH inhibition activates TLR‑VCAM1 pathway and suppresses the development of MLL‑fusion leukemia | | 10 | 2017 | 24 | The ubiquitin ligase STUB1 regulates stability and activity of RUNX1 and RUNX1–RUNX1T1 | | 11 | 2019 | 23 | Autophagy induction by xanthoangelol exhibits anti‑metastatic activities in hepatocellular carcinoma | | 12 | 2019 | 21 | Oncogenic ERBB2 Aberrations and KRAS Mutations Cooperate to Promote Pancreatic Ductal Adenocarcinoma Progression. | | 13 | 2019 | 12 | Opposing effects of acute versus chronic inhibition of p53 on decitabine’s efficacy in myeloid neoplasms | | 14 | 2020 | 11 | The nuclear localized RIN13 induces cell death through interacting with ARF1. | | 15 | 2020 | 10 | RIN13-mediated disease resistance depends on SNC1-EDS1/PAD4 signaling pathway in Arabidopsis. | | 16 | 2023 | 7 | METTL3 regulatory TROAP can regulate the progression of non-small cell lung cancer through PI3K/AKT and EMT signaling pathway | | 17 | 2013 | 5 | The effects of C60(C(COOH)2)2-FITC on proliferation and differentiation of human mesenchymal stem cells in vitro. | | 18 | 2023 | 5 | Blocking sphingosine 1-phosphate receptor 1 with modulators reduces immune cells infiltration and alleviates endometriosis in mice. | | 19 | 2018 | 4 | miRNA ‐ 199 a ‐ 5 p suppresses proliferation and invasion by directly targeting NF ‐ κ B 1 in human ovarian cancer cells | | 20 | 2005 | 0 | HER4 Expression is Altered by Radiation in Clinical Breast Cancers, and Induces Radiosensitization in Vitro in a Breast Cancer Cell Line |