Dynamic Weighting Translation Transfer Learning for Imbalanced Medical Image Classification.

Medical image diagnosis using deep learning has shown significant promise in clinical medicine. However, it often encounters two major difficulties in real-world applications: (1) domain shift, which invalidates the trained model on new datasets, and (2) class imbalance problems leading to model biases towards majority classes. To address these challenges, this paper proposes a transfer learning solution, named Dynamic Weighting Translation Transfer Learning (DTTL), for imbalanced medical image classification. The approach is grounded in information and entropy theory and comprises three modules: Cross-domain Discriminability Adaptation (CDA), Dynamic Domain Translation (DDT), and Balanced Target Learning (BTL). CDA connects discriminative feature learning between source and target domains using a synthetic discriminability loss and a domain-invariant feature learning loss. The DDT unit develops a dynamic translation process for imbalanced classes between two domains, utilizing a confidence-based selection approach to select the most useful synthesized images to create a pseudo-labeled balanced target domain. Finally, the BTL unit performs supervised learning on the reassembled target set to obtain the final diagnostic model. This paper delves into maximizing the entropy of class distributions, while simultaneously minimizing the cross-entropy between the source and target domains to reduce domain discrepancies. By incorporating entropy concepts into our framework, our method not only significantly enhances medical image classification in practical settings but also innovates the application of entropy and information theory within deep learning and medical image processing realms. Extensive experiments demonstrate that DTTL achieves the best performance compared to existing state-of-the-art methods for imbalanced medical image classification tasks.

Affine Iterative Closest Point Algorithm Based on Color Information and Correntropy for Precise Point Set Registration.

In this paper, we propose a novel affine iterative closest point algorithm based on color information and correntropy, which can effectively deal with the registration problems with a large number of noise and outliers and small deformations in RGB-D datasets. Firstly, to alleviate the problem of low registration accuracy for data with weak geometric structures, we consider introducing color features into traditional affine algorithms to establish more accurate and reliable correspondences. Secondly, we introduce the correntropy measurement to overcome the influence of a large amount of noise and outliers in the RGB-D datasets, thereby further improving the registration accuracy. Experimental results demonstrate that the proposed registration algorithm has higher registration accuracy, with error reduction of almost 10 times, and achieves more stable robustness than other advanced algorithms.

Semiconducting polymer nano-radiopharmaceutical for combined radio-photothermal therapy of pancreatic tumor.

BACKGROUND: Pancreatic ductal adenocarcinoma (PDAC) is a devastatingly malignant tumor with a high mortality. However, current strategies to treat PDAC generally have low efficacy and high side-effects, therefore, effective treatment against PDAC remains an urgent need. RESULTS: We report a semiconducting polymer nano-radiopharmaceutical with intrinsic photothermal capability and labeling with therapeutic radioisotope 177Lu (177Lu-SPN-GIP) for combined radio- and photothermal therapy of pancreatic tumor. 177Lu-SPN-GIP endowed good stability at physiological conditions, high cell uptake, and long retention time in tumor site. By virtue of combined radiotherapy (RT) and photothermal therapy (PTT), 177Lu-SPN-GIP exhibited enhanced therapeutic capability to kill cancer cells and xenograft tumor in living mice compared with RT or PTT alone. More importantly, 177Lu-SPN-GIP could suppress the growth of the tumor stem cells and reverse epithelial mesenchymal transition (EMT), which may greatly reduce the occurrence of metastasis. CONCLUSION: Such strategy we developed could improve therapeutic outcomes over traditional RT as it is able to ablate tumor with relatively lower doses of radiopharmaceuticals to reduce its side effects.

Long Non-Coding RNA CRYBG3 Promotes Lung Cancer Metastasis via Activating the eEF1A1/MDM2/MTBP Axis.

The occurrence of distant tumor metastases is a major barrier in non-small cell lung cancer (NSCLC) therapy, and seriously affects clinical treatment and patient prognosis. Recently, long non-coding RNAs (lncRNAs) have been demonstrated to be crucial regulators of metastasis in lung cancer. The aim of this study was to reveal the underlying mechanisms of a novel lncRNA LNC CRYBG3 in regulating NSCLC metastasis. Experimental results showed that LNC CRYBG3 was upregulated in NSCLC cells compared with normal tissue cells, and its level was involved in these cells' metastatic ability. Exogenously overexpressed LNC CRYBG3 increased the metastatic ability and the protein expression level of the metastasis-associated proteins Snail and Vimentin in low metastatic lung cancer HCC827 cell line. In addition, LNC CRYBG3 contributed to HCC827 cell metastasis in vivo. Mechanistically, LNC CRYBG3 could directly combine with eEF1A1 and promote it to move into the nucleus to enhance the transcription of MDM2. Overexpressed MDM2 combined with MDM2 binding protein (MTBP) to reduce the binding of MTBP with ACTN4 and consequently increased cell migration mediated by ACTN4. In conclusion, the LNC CRYBG3/eEF1A1/MDM2/MTBP axis is a novel signaling pathway regulating tumor metastasis and may be a potential therapeutic target for NSCLC treatment.

Circadian effects of ionizing radiation on reproductive function and clock genes expression in male mouse.

BACKGROUND: Exposure to the ionizing radiation (IR) encountered outside the magnetic field of the Earth poses a persistent threat to the reproductive functions of astronauts. The potential effects of space IR on the circadian rhythms of male reproductive functions have not been well characterized so far. METHODS: Here, we investigated the circadian effects of IR exposure (3 Gy X-rays) on reproductive functional markers in mouse testicular tissue and epididymis at regular intervals over a 24-h day. For each animal, epididymis was tested for sperm motility, and the testis tissue was used for daily sperm production (DSP), testosterone levels, and activities of testicular enzymes (glucose-6-phosphate dehydrogenase (G6PDH), sorbitol dehydrogenase (SDH), lactic dehydrogenase (LDH), and acid phosphatase (ACP)), and the clock genes mRNA expression such as Clock, Bmal1, Ror-α, Ror-ß, or Ror-γ. RESULTS: Mice exposed to IR exhibited a disruption in circadian rhythms of reproductive markers, as indicated by decreased sperm motility, increased daily sperm production (DSP), and reduced activities of testis enzymes such as G6PDH, SDH, LDH, and ACP. Moreover, IR exposure also decreased mRNA expression of five clock genes (Clock, Bmal1, Ror-α, Ror-ß, or Ror-γ) in testis, with alteration in the rhythm parameters. CONCLUSION: These findings suggested potential health effects of IR exposure on reproductive functions of male astronauts, in terms of both the daily overall level as well as the circadian rhythmicity.

Microarray Profiling of TGF-ß1-Induced Long Non-Coding RNA Expression Patterns in Human Lung Bronchial Epithelial BEAS-2B Cells.

BACKGROUND/AIMS: TGF-ß1 mediated radiation-induced bystander effects (RIBE) have been linked with malignant transformation and tumorigenesis. However, the underlying mechanisms are not fully understood. METHODS: To reveal new molecules of regulatory functions in this process, lncRNA microarray was performed to profile both lncRNA and mRNA expression patterns in human lung bronchial epithelial BEAS-2B cells treated with TGF-ß1 at a concentration measured in the medium conditioned by directly irradiated BEAS-2B cells. The potential functions of the differentially expressed lncRNAs were predicted by GO and KEGG pathway analyses of their co-expressed mRNAs. Cis- and trans-regulation of the lncRNAs were analyzed and the interaction networks were constructed using Cytoscape. qRT-PCR was conducted to validate the results of microarray profiling. CCK-8 assay was employed for functional validation of 3 identified lncRNAs. RESULTS: 224 lncRNAs were found to be dysregulated, among which 6 lncRNAs were chosen for expression validation by qRT-PCR assay. Pathway analyses showed that differentially expressed lncRNAs are highly correlated with cell proliferation, transformation, migration, etc. Trans-regulation analyses showed that the differentially expressed lncRNAs most likely participate in the pathways regulated by four transcriptional factors, FOS, STAT3, RAD21 and E2F1, which have been identified to be involved in the modulation of oncogenic transformation, cell cycle progression, genomic instability, etc. lnc-THEMIS-2 and lnc-ITGB6-4, predicted to be regulated by STAT3 and E2F1 respectively, were found to rescue the decrease of cell viability induced by TGF-ß1 treatment. CONCLUSION: Our findings suggest that the differentially expressed lncRNAs induced by TGF-ß1 play crucial roles in the oncogenic transformation and tumorigenesis, which provide a better understanding of the underlying mechanisms related to tumorigensis induced by LD/LDR radiations.

Therapeutic ionizing radiation induced bone loss: a review of in vivo and in vitro findings.

Radiation therapy is one of the routine treatment modalities for cancer patients. Ionizing radiation (IR) can induce bone loss, and consequently increases the risk of fractures with delayed and nonunion of the bone in the cancer patients who receive radiotherapy. The orchestrated bone remodeling can be disrupted due to the affected behaviors of bone cells, including bone mesenchymal stem cells (BMSCs), osteoblasts and osteoclasts. BMSCs and osteoblasts are relatively radioresistant compared with osteoclasts and its progenitors. Owing to different radiosensitivities of bone cells, unbalanced bone remodeling caused by IR is closely associated with the dose absorbed. For doses less than 2 Gy, osteoclastogenesis and adipogenesis by BMSCs are enhanced, while there are limited effects on osteoblasts. High doses (>10 Gy) induce disrupted architecture of bone, which is usually related to decreased osteogenic potential. In this review, studies elucidating the biological effects of IR on bone cells (BMSCs, osteoblasts and osteoclasts) are summarized. Several potential preventions and therapies are also proposed.

MiR-21 is involved in radiation-induced bystander effects.

Radiation-induced bystander effects are well-established phenomena, in which DNA damage responses are induced not only in the directly irradiated cells but also in the non-irradiated bystander cells through intercellular signal transmission. Recent studies hint that bystander effects are possibly mediated via small non-coding RNAs, especially microRNAs. Thus, more details about the roles of microRNA in bystander effects are urgently needed to be elucidated. Here we demonstrated that bystander effects were induced in human fetal lung MRC-5 fibroblasts through medium-mediated way by different types of radiation. We identified a set of differentially expressed microRNAs in the cell culture medium after irradiation, among which the up-regulation of miR-21 was further verified with qRT-PCR. In addition, we found significant upregulation of miR-21 in both directly irradiated cells and bystander cells, which was confirmed by the expression of miR-21 precursor and its target genes. Transfection of miR-21 mimics into non-irradiated MRC-5 cells caused bystander-like effects. Taken together, our data reveals that miR-21 is involved in radiation-induced bystander effects. Elucidation of such a miRNA-mediated bystander effect is of utmost importance in understanding the biological processes related to ionizing radiation and cell-to-cell communication.

MiR-663 inhibits radiation-induced bystander effects by targeting TGFB1 in a feedback mode.

The mechanisms of radiation-induced bystander effects (RIBE) have been investigated intensively over the past two decades. Although quite a few reports demonstrated that cytokines such as TGF-ß1 are induced within the directly irradiated cells and play critical roles in mediating the bystander effects, little is known about the signaling pathways that occur in bystander cells. The crucial question as to why RIBE signals cannot be infinitely transmitted, therefore, remains unclear. In the present study, we showed that miR-663, a radiosensitive microRNA, participates in the regulation of biological effects in both directly irradiated and bystander cells via its targeting of TGF-ß1. MiR-663 was downregulated, while TGFB1 was upregulated in directly irradiated cells. The regulation profile of miR-663 and TGFB1, on the other hand, was reversed in bystander cells, in which an elevated miR-663 expression was exhibited and led to downregulation of TGF-ß1. Further studies revealed that miR-663 interacts with TGFB1 directly and that through its binding to the core regulation sequence, miR-663 suppresses the expression of TGFB1. Based on the results, we propose that miR-663 inhibits the propagation of RIBE in a feedback mode, in which the induction of TGF-ß1 by reduced miR-663 in directly irradiated cells leads to increased level of miR-663 in bystander cells. The upregulation of miR-663 in turn suppresses the expression of TGF-ß1 and limits further transmission of the bystander signals.

Compound Learning-Based Model Predictive Control Approach for Ducted-Fan Aerial Vehicles.

Designing an efficient learning-based model predictive control (MPC) framework for ducted-fan unmanned aerial vehicles (DFUAVs) is a difficult task due to several factors involving uncertain dynamics, coupled motion, and unorthodox aerodynamic configuration. Existing control techniques are either developed from largely known physics-informed models or are made for specific goals. In this regard, this article proposes a compound learning-based MPC approach for DFUAVs to construct a suitable framework that exhibits efficient dynamics learning capability with adequate disturbance rejection characteristics. At the start, a nominal model from a largely unknown DFUAV model is achieved offline through sparse identification. Afterward, a reinforcement learning (RL) mechanism is deployed online to learn a policy to facilitate the initial guesses for the control input sequence. Thereafter, an MPC-driven optimization problem is developed, where the obtained nominal (learned) system is updated by the real system, yielding improved computational efficiency for the overall control framework. Under appropriate assumptions, stability and recursive feasibility are compactly ensured. Finally, a comparative study is conducted to illustrate the efficacy of the designed scheme.

X-ray-downregulated nucleophosmin induces abnormal polarization by anchoring to G-actin.

Ionizing radiation poses significant risks to astronauts during deep space exploration. This study investigates the impact of radiation on nucleophosmin (NPM), a protein involved in DNA repair, cell cycle regulation, and proliferation. Using X-rays, a common space radiation, we found that radiation suppresses NPM expression. Knockdown of NPM increases DNA damage after irradiation, disrupts cell cycle distribution and enhances cellular radiosensitivity. Additionally, NPM interacts with globular actin (G-actin), affecting its translocation and centrosome binding during mitosis. These findings provide insights into the role of NPM in cellular processes in responding to radiation. This article enhances our comprehension of radiation-induced genomic instability and provides a foundational platform for prospective investigations within the realm of space radiation and its implications for cancer therapy.

YBX1 Underwent Phase Separation into Stress Granules Stimulated by Ionizing Radiation.

Stress granules (SGs) are formed through liquid-liquid phase separation (LLPS), in response to external stimuli. YBX1, an integral component of SGs, plays a crucial role in tumor progression and cellular stress response. This study aims to elucidate the mechanisms and specific biological implications of YBX1 in SG formation, along with the identification of key regions and interacting proteins. Our observations indicate that YBX1 rapidly undergoes liquid-liquid phase separation, leading to SG formation in response to 8 Gy X-ray irradiation within 1 h, with SGs reverting to their original state after 5 h. There was a potential interaction between ATXN2L and YBX1, persisting YBX1 within the SGs. Our data suggested a potential interaction between ATXN2L and YBX1, and it remained associated with YBX1 within the SGs. Furthermore, our subsequent studies demonstrate that targeting ATXN2L can diminish the recruitment of YBX1 to stress granules (SGs), consequently enhancing the radiosensitivity of HeLa cells.

Emerging roles of long noncoding RNAs in enzymes related intracellular metabolic pathways in cancer biology.

Metabolic reprogramming plays critical roles in the development and progression of tumor by providing cancer cells with a sufficient supply of nutrients and other factors needed for fast-proliferating. Emerging evidence indicates that long noncoding RNAs (lncRNAs) are involved in the initiation of metastasis via regulating the metabolic reprogramming in various cancers. In this paper, we aim to summarize that lncRNAs could participate in intracellular nutrient metabolism including glucose, amino acid, lipid, and nucleotide, regardless of whether lncRNAs have tumor-promoting or tumor-suppressor function. Meanwhile, modulation of lncRNAs in glucose metabolic enzymes in glycolysis, pentose phosphate pathway and tricarboxylic acid cycle (TCA) in cancer is reviewed. We also discuss therapeutic strategies targeted at interfering with enzyme activity to decrease the utilization of glucoses, amino acid, nucleotide acid and lipid in tumor cells. This review focuses on our current understanding of lncRNAs participating in cancer cell metabolic reprogramming, paving the way for further investigation into the combination of such approaches with existing anti-cancer therapies.

Activated PARP1/FAK/COL5A1 signaling facilitates the tumorigenesis of cholesterol-resistant ovarian cancer cells through promoting EMT.

Cancer cells require plentiful cholesterol for membrane biogenesis and other functional needs due to fast proliferating, leading to the interaction of cholesterol or its metabolites with cancer-related pathways. However, the impact of long-lasting high cholesterol concentrations on tumorigenesis and its underlying mechanisms remains largely unexplored. To the best of our knowledge, this study is the first to establish a cholesterol-resistant ovarian cancer cells, whose intracellular total cholesterol level up to 6-8 mmol/L. We confirmed that high cholesterol facilitated the progression of ovarian cancer in vitro and in vivo. Notably, our findings revealed significant upregulation of collagen type V alpha 1 chain (COL5A1) expression in cholesterol-resistant ovarian cancer cells and human ovarian cancer tissue, which was depended on FAK/Src activation. Mechanistically, PARP1 directly bound to FAK in response to activate FAK/Src/COL5A1 signaling. Intriguingly, COL5A1 depletion significantly impeded the tumorigenesis of these cells, concomitant with a decrease in epithelial-mesenchymal transition (EMT) progression. In conclusion, PARP1/FAK/COL5A1 signaling activation facilitated progression of cholesterol-resistant ovarian cancer cells by promoting EMT, thereby broadening a new therapeutic opportunity.

Engineered bacteria breach tumor physical barriers to enhance radio-immunotherapy.

Radiotherapy widely applied for local tumor therapy in clinic has been recently reinvigorated by the discovery that radiotherapy could activate systematic antitumor immune response. Nonetheless, the endogenous radio-immune effect is still incapable of radical tumor elimination due to the prevention of immune cell infiltration by the physical barrier in tumor microenvironment (TME). Herein, an engineered Salmonella secreting nattokinase (VNPNKase) is developed to synergistically modulate the physical and immune characteristics of TME to enhance radio-immunotherapy of colon tumors. The facultative anaerobic VNPNKase enriches at the tumor site after systemic administration, continuously secreting abundant NKase to degrade fibronectin, dredge the extracellular matrix (ECM), and inactivate cancer-associated fibroblasts (CAFs). The VNPNKase- dredged TME facilitates the infiltration of CD103+ dendritic cells (DCs) and thus the presentation of tumor-associated antigens (TAAs) after radiotherapy, recruiting sufficient CD8+ T lymphocytes to specifically eradicate localized tumors. Moreover, the pre-treatment of VNPNKase before radiotherapy amplifies the abscopal effect and achieves a long-term immune memory effect, preventing the metastasis and recurrence of tumors. Our research suggests that this strategy using engineered bacteria to breach tumor physical barrier for promoting immune cell infiltration possesses great promise as a translational strategy to enhance the effectiveness of radio-immunotherapy in treating solid tumors.

Dynamic Graph Clustering Learning for Unsupervised Diabetic Retinopathy Classification.

Diabetic retinopathy (DR) is a common complication of diabetes, which can lead to vision loss. Early diagnosis is crucial to prevent the progression of DR. In recent years, deep learning approaches have shown promising results in the development of an intelligent and efficient system for DR classification. However, one major drawback is the need for expert-annotated datasets, which are both time-consuming and costly. To address these challenges, this paper proposes a novel dynamic graph clustering learning (DGCL) method for unsupervised classification of DR, which innovatively deploys the Euclidean and topological features from fundus images for dynamic clustering. Firstly, a multi-structural feature fusion (MFF) module extracts features from the structure of the fundus image and captures topological relationships among multiple samples, generating a fused representation. Secondly, another consistency smoothing clustering (CSC) module combines network updates and deep clustering to ensure stability and smooth performance improvement during model convergence, optimizing the clustering process by iteratively updating the network and refining the clustering results. Lastly, dynamic memory storage is utilized to track and store important information from previous iterations, enhancing the training stability and convergence. During validation, the experimental results with public datasets demonstrated the superiority of our proposed DGCL network.

The role of bacteria and its derived biomaterials in cancer radiotherapy.

Bacteria-mediated anti-tumor therapy has received widespread attention due to its natural tumor-targeting ability and specific immune-activation characteristics. It has made significant progress in breaking the limitations of monotherapy and effectively eradicating tumors, especially when combined with traditional therapy, such as radiotherapy. According to their different biological characteristics, bacteria and their derivatives can not only improve the sensitivity of tumor radiotherapy but also protect normal tissues. Moreover, genetically engineered bacteria and bacteria-based biomaterials have further expanded the scope of their applications in radiotherapy. In this review, we have summarized relevant researches on the application of bacteria and its derivatives in radiotherapy in recent years, expounding that the bacteria, bacterial derivatives and bacteria-based biomaterials can not only directly enhance radiotherapy but also improve the anti-tumor effect by improving the tumor microenvironment (TME) and immune effects. Furthermore, some probiotics can also protect normal tissues and organs such as intestines from radiation via anti-inflammatory, anti-oxidation and apoptosis inhibition. In conclusion, the prospect of bacteria in radiotherapy will be very extensive, but its biological safety and mechanism need to be further evaluated and studied.

Large-scale ORF screening based on LC-MS to discover novel lncRNA-encoded peptides responding to ionizing radiation and microgravity.

In the human genome, 98% of genes can be transcribed into non-coding RNAs (ncRNAs), among which lncRNAs and their encoded peptides play important roles in regulating various aspects of cellular processes and may serve as crucial factors in modulating the biological effects induced by ionizing radiation and microgravity. Unfortunately, there are few reports in space radiation biology on lncRNA-encoded peptides below 10kD due to limitations in detection techniques. To fill this gap, we integrated a variety of methods based on genomics and peptidomics, and discovered 22 lncRNA-encoded small peptides that are sensitive to space radiation and microgravity, which have never been reported before. We concurrently validated the transmembrane helix, subcellular localization, and biological function of these small peptides using bioinformatics and molecular biology techniques. More importantly, we found that these small peptides function independently of the lncRNAs that encode them. Our findings have uncovered a previously unknown human proteome encoded by 'non-coding' genes in response to space conditions and elucidated their involvement in biological processes, providing valuable strategies for individual protection mechanisms for astronauts who carry out deep space exploration missions in space radiation environments.

The Tumorigenic Effect of lncRNA AFAP1-AS1 is Mediated by Translated Peptide ATMLP Under the Control of m6 A Methylation.

Long noncoding RNAs (lncRNAs) in eukaryotic transcripts have long been believed to regulate various aspects of cellular processes, including carcinogenesis. Herein, it is found that lncRNA AFAP1-AS1 encodes a conserved 90-amino acid peptide located on mitochondria, named lncRNA AFAP1-AS1 translated mitochondrial-localized peptide (ATMLP), and it is not the lncRNA but the peptide that promotes the malignancy of nonsmall cell lung cancer (NSCLC). As the tumor progresses, the serum level of ATMLP increases. NSCLC patients with high levels of ATMLP display poorer prognosis. Translation of ATMLP is controlled by m6 A methylation at the 1313 adenine locus of AFAP1-AS1. Mechanistically, ATMLP binds to the 4-nitrophenylphosphatase domain and non-neuronal SNAP25-like protein homolog 1 (NIPSNAP1) and inhibits its transport from the inner to the outer mitochondrial membrane, which antagonizes the NIPSNAP1-mediated regulation of cell autolysosome formation. The findings uncover a complex regulatory mechanism of NSCLC malignancy orchestrated by a peptide encoded by a lncRNA. A comprehensive judgment of the application prospects of ATMLP as an early diagnostic biomarker for NSCLC is also made.

Downregulation of Long Noncoding RNA CRYBG3 Enhances Radiosensitivity in Non-Small Cell Lung Cancer Depending on p53 Status.

Non-small cell lung cancer (NSCLC) is the most common type of lung cancer with high recurrence and metastasis rates, and more than half of the patients diagnosed with NSCLC receive local radiotherapy. However, the intrinsic radio-resistance of cancer cells is a major barrier to effective radiotherapy for NSCLC. CRYBG3 is a long noncoding RNA (lncRNA) that was originally identified to be upregulated in NSCLC and enhanced metastasis of NSCLC cells by interacting with eEF1A1 to promote murine double minute 2 (MDM2) expression. The aims of this study were to reveal the contribution of CRYBG3 to the radioresistance of NSCLC and determine whether that is associated with MDM2-p53 pathway. Therefore, CRYBG3 was stably downregulated in A549 (wild-type p53) and H1299 (deficient p53) cells by infecting short hairpin RNA (shRNA) lentiviral particles. The results showed that downregulation of CRYBG3 increased DNA damage, enhanced apoptosis and pro-apoptotic protein expression in A549 or p53-overexpressed H1299 cells but not in H1299 or p53-silenced A549 cells after X-ray irradiation. However, the contribution of CRYBG3 to radioresistance was abolished by eEF1A1 or MDM2 knockdown in A549 cells. Thus, we concluded that downregulation of CRYBG3 enhanced radiosensitivity by reducing MDM2 expression then leading to decreased MDM2-mediated degradation of p53 in wild-type p53 expressing NSCLC cells. These findings suggested that CRYBG3 can be a potential target for therapeutic intervention of certain lung cancer subtypes.